The DOI matches its Crossref record; 87 of the 87 references it cites were found in a registry or an index; none of the 105 sources its claims cite is checked for support yet.
Principles and clinical implications of the brain-gut-enteric microbiota axis
Open accessAbstract
While bidirectional brain–gut interactions are well known mechanisms for the regulation of gut function in both healthy and diseased states, a role of the enteric flora—including both commensal and pathogenic organisms—in these interactions has only been recognized in the past few years. The brain can influence commensal organisms (enteric microbiota) indirectly, via changes in gastrointestinal motility and secretion, and intestinal permeability, or directly, via signaling molecules released into the gut lumen from cells in the lamina propria (enterochromaffin cells, neurons, immune cells). Communication from enteric microbiota to the host can occur via multiple mechanisms, including epithelial-cell, receptor-mediated signaling and, when intestinal permeability is increased, through direct stimulation of host cells in the lamina propria. Enterochromaffin cells are important bidirectional transducers that regulate communication between the gut lumen and the nervous system. Vagal, afferent innervation of enterochromaffin cells provides a direct pathway for enterochromaffin-cell signaling to neuronal circuits, which may have an important role in pain and immune-response modulation, control of background emotions and other homeostatic functions. Disruption of the bidirectional interactions between the enteric microbiota and the nervous system may be involved in the pathophysiology of acute and chronic gastrointestinal disease states, including functional and inflammatory bowel disorders.
Overview
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Written from the paper’s full text.
TL;DR
This review synthesizes evidence for bidirectional signaling between the CNS and the enteric microbiota—the "brain–gut–enteric microbiota axis"—and proposes enterochromaffin cells as key bidirectional transducers. It argues that disruption of these interactions may contribute to functional and inflammatory bowel disorders, though causative roles remain unproven.
Key findings
- The brain can influence commensal organisms indirectly (via ANS-mediated changes in motility, secretion, and intestinal permeability) and directly via signaling molecules (catecholamines, serotonin, dynorphin, cytokines) released into the gut lumen from neurons, immune cells, and enterochromaffin cells.
- Microbe-to-host signaling occurs via epithelial receptor-mediated mechanisms (e.g., Toll-like receptors) and, when permeability is increased, through direct stimulation of lamina propria cells; the autoinducer-3–QseC system in enterohemorrhagic *E. coli* is activated by host norepinephrine, enabling interkingdom signaling during stress.
- Enterochromaffin cells are positioned to act as bidirectional transducers: they secrete serotonin and peptides in response to luminal microbial factors and central stimuli, and vagal afferents expressing 5-HT3R lie in close proximity.
- Germ-free mice showed less intense inflammation-associated hyperalgesia than conventional mice, associated with increased interleukin-10 expression, reversed by anti-interleukin-10 antibody; the human gut harbors 400–1,000 bacterial species with ~10¹¹ bacterial cells per gram of colon contents.
- Two cited RCTs: 4-week *Bifidobacterium lactis* reduced abdominal distention and accelerated orocecal/colonic transit in IBS with constipation; 8-week *Bifidobacterium infantis* improved symptoms and normalized the plasma IL-10:IL-12 ratio.
Methods
- Narrative review (not a primary study) summarizing preclinical and clinical evidence on bidirectional nervous system–enteric microbiota interactions.
- Draws on animal models (rhesus monkeys, mice, rats, pigs), in vitro studies, and human clinical trials, including cited randomized controlled trials of probiotics in IBS.
- Organizes evidence into brain-to-microbiota signaling, microbe-to-gut-to-brain signaling, enterochromaffin cell transduction, vagal transmission, homeostatic functions, and clinical/therapeutic implications.
Limitations
- The paper states that evidence is "often sparse," that host-to-enteric bacteria signaling has been characterized in detail only for pathogenic organisms and only for some molecules (norepinephrine, dynorphins, cytokines), and that considerably more data are needed to establish a causative role for microbiota changes in IBS symptoms.
- The paper notes most studies of CNS influence on microbiota used luminal bacterial populations from stool samples, with biofilm-adjacent organisms less well documented.
- Evident from the text: this is a review without primary data or systematic search methodology, and several proposed mechanisms (e.g., enterochromaffin cell signaling to brain function, adrenergic receptors on epithelial brush border) are explicitly described as not yet studied in detail.
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Claims the paper makes
72 Not checked yet · 40 Own interpretation · 1 No basis given
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In the paper
“the mechanisms that underlie the observed effects are poorly understood.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Introduction
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In the paper
“The enteric microbiota can directly influence gut homeostasis by the regulation of bowel motility and modulation of intestinal pain, immune responses, and nutrient processing.8-10”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Introduction
What the sources say
- Not checked yetcites [8] Husebye, E., Hellstrom, P. M., Sundler, F., Chen, J. & Midtvedt, T. Influence of microbial species on small intestinal myoelectric activity and transit in germ-free rats. Am. J. Physiol. Gastrointest. Liver Physiol. 280, G368–G380 (2001). source
- Not checked yetcites [9] Rhee, S. H. et al. Pathophysiological role of Toll-like receptor 5 engagement by bacterial flagellin in colonic inflammation. Proc. Natl Acad. Sci. USA 102, 13610–13615 (2005). source
- Not checked yetcites [10] Ait-Belgnaoui, A. et al. Lactobacillus farciminis treatment suppresses stress induced visceral hypersensitivity: a possible action through interaction with epithelial cell cytoskeleton contraction. Gut 55, 1090–1094 (2006). source
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In the paper
“Enterochromaffin cells are important bidirectional transducers that regulate communication between the gut lumen and the nervous system.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Abstract
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In the paper
“while accelerated intestinal transit, with an increased number of giant, migrating contractions, is seen in many diarrheal states, including diarrhea-predominant IBS.22”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS-related changes in gut environment
What the sources say
- Not checked yetcites [22] Chey, W. Y. et al. Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea. Am. J. Gastroenterol. 96, 1499–1506 (2001). source
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In the paper
“Impaired intestinal transit caused by compromised, migrating motor complexes (a motor pattern characteristic of the fasting state of the gastrointestinal tract that is under parasympathetic control), is associated with bacterial overgrowth in the small intestine.20”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS-related changes in gut environment
What the sources say
- Not checked yetcites [20] Van Felius, I. D. et al. Interdigestive small bowel motility and duodenal bacterial overgrowth in experimental acute pancreatitis. Neurogastroenterol. Motil. 15, 267–276 (2003). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Different types of psychological stressors modulate the composition and total biomass of the enteric microbiota in both adult15 and newborn animals.16”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
What the sources say
- Not checked yetcites [15] Schaedler, R. W. & Dubos, R. J. The fecal flora of various strains of mice. Its bearing on their susceptibility to endotoxin. J. Exp. Med. 115, 1149–1160 (1962). source
- Not checked yetcites [16] Bailey, M. T. & Coe, C. L. Maternal separation disrupts the integrity of the intestinal microflora in infant rhesus monkeys. Dev. Psychobiol. 35, 146–155 (1999). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In this case, the shedding of lactobacilli may have been related to the stress-induced acceleration of intestinal transit, since normal bacterial levels were restored 1 week after separation.16”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
What the sources say
- Not checked yetcites [16] Bailey, M. T. & Coe, C. L. Maternal separation disrupts the integrity of the intestinal microflora in infant rhesus monkeys. Dev. Psychobiol. 35, 146–155 (1999). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Although different types of psychological stressors, including early-life stress and sustained stress, have been recognized as risk factors or promoters of events that result in disease exacerbation in patients with ulcerative colitis2 and IBS,3”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Introduction
What the sources say
- Not checked yetcites [2] Levenstein, S. et al. Stress and exacerbation in ulcerative colitis: a prospective study of patients enrolled in remission. Am. J. Gastroenterol. 95, 1213–1220 (2000). source
- Not checked yetcites [3] Whitehead, W. E., Crowell, M. D., Robinson, J. C., Heller, B. R. & Schuster, M. M. Effects of stressful life events on bowel symptoms: subjects with irritable bowel syndrome compared with subjects without bowel dysfunction. Gut 33, 825–830 (1992). source
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The activation of any of these systems, either alone or in combination, might influence enteric microbiota both indirectly, via changes in their environment, and directly, via host–enteric microbiota signaling.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
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In the paper
“Both sympathetic and parasympathetic nervous systems, which are part of the ANS, have a prominent role in the modulation of gut functions, such as motility, secretion of acid, bicarbonates and mucus, intestinal-fluid handling and mucosal immune response (reviewed elsewhere1).”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS-related changes in gut environment
What the sources say
- Not checked yetcites [1] Mayer, E. A. The neurobiology of stress and gastrointestinal disease. Gut 47, 861–869 (2000). source
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 31
- Probably not a substantial claim. 13
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The brain can influence commensal organisms (enteric microbiota) indirectly, via changes in gastrointestinal motility and secretion, and intestinal permeability, or directly, via signaling molecules released into the gut lumen from cells in the lamina propria (enterochromaffin cells, neurons, immune cells).”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In maternal separation-induced, postnatal stress, reduction in lactobacilli was associated with the appearance of stress-indicative behaviors, and affected animals were more susceptible than unstressed controls to opportunistic infection.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
What the sources say
- Not checked yetcites [16] Bailey, M. T. & Coe, C. L. Maternal separation disrupts the integrity of the intestinal microflora in infant rhesus monkeys. Dev. Psychobiol. 35, 146–155 (1999). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Vagal, afferent innervation of enterochromaffin cells provides a direct pathway for enterochromaffin-cell signaling to neuronal circuits, which may have an important role in pain and immune-response modulation, control of background emotions and other homeostatic functions.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the role of the enteric microbiota in bidirectional gut–brain interactions in health and disease has received little attention until the past 5 years or so.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Introduction
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“Both pre natal17 and postnatal stress16 were associated with transient reductions in the levels of the enteric microbiota in rhesus monkeys.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
What the sources say
- Not checked yetcites [17] Bailey, M. T. et al. Prenatal stress alters bacterial colonization of the gut in infant monkeys. J. Pediatr. Gastroenterol. Nutr. 38, 414–421 (2004). source
- Not checked yetcites [16] Bailey, M. T. & Coe, C. L. Maternal separation disrupts the integrity of the intestinal microflora in infant rhesus monkeys. Dev. Psychobiol. 35, 146–155 (1999). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In general, bacteria located in the biofilm seem to be less affected by environmental alterations, such as changes in intestinal transit rate and luminal contents, than luminal populations are, but seem to have increased involvement in bidirectional signaling with the host.19”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
What the sources say
- Not checked yetcites [19] Macfarlane, S. & Dillon, J. F. Microbial biofilms in the human gastrointestinal tract. J. Appl. Microbiol. 102, 1187–1196 (2007). source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, several studies have demonstrated that stressful stimuli can enhance the permeability of the intestinal epithelium, which allows bacterial antigens to penetrate the gut epithelium and triggers an immune response in the intestinal mucosa.23-27”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS-related changes in gut environment
What the sources say
- Not checked yetcites [23] Kiliaan, A. J. et al. Stress stimulates transepithelial macromolecular uptake in rat jejunum. Am. J. Physiol. 275, G1037–G1044 (1998).
- Not checked yetcites [24] Groot, J. et al. Stress-induced decrease of the intestinal barrier function. The role of muscarinic receptor activation. Ann. NY Acad. Sci. 915, 237–246 (2000). source
- Not checked yetcites [25] Yates, D. A., Santos, J., Soderholm, J. D. & Perdue, M. H. Adaptation of stress-induced mucosal pathophysiology in rat colon involves opioid pathways. Am. J. Physiol. Gastrointest. Liver Physiol. 281, G124–G128 (2001). source
- Not checked yetcites [26] Soderholm, J. D. et al. Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress. Am. J. Physiol. Gastrointest. Liver Physiol. 283, G1257–G1263 (2002). source
- Not checked yetcites [27] Jacob, C. et al. Mast cell tryptase controls paracellular permeability of the intestine. Role of protease-activated receptor 2 and beta-arrestins. J. Biol. Chem. 280, 31936–31948 (2005). source
boosteddirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The ANS also affects epithelial mechanisms involved in immune activation of the gut, either directly, through modulation of the response of the gut immune cells (for example, macrophages and mast cells) to luminal bacteria, or indirectly, through alteration of the access of luminal bacteria to gut immunocytes (Figure 2).”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS-related changes in gut environment
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In the paper
“Notably, most of the studies that have examined the influence of these systems on enteric microbiota have been performed on luminal bacterial populations from stool samples, whereas the influence of these systems on organisms contained in the biofilm adjacent to the intestinal mucosa are less well documented.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Brain to enteric microbiota signaling
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In the paper
“For example, serotonin secretion into the stomach lumen has been reported in response to an intrathecal injection into the cerebrospinal fluid (central injection) of TRP, an analog of thyrotropin-releasing hormone, which is a central mediator of the stress response to cold temperatures.31,32 This secretion is probably mediated by vagal activation of gastric enterochromaffin cells.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS modulation of gut–microbe signaling
What the sources say
- Not checked yetcites [31] Stephens, R. L. & Tache, Y. Intracisternal injection of a TRH analogue stimulates gastric luminal serotonin release in rats. Am. J. Physiol. 256, G377–G383 (1989).
- Not checked yetcites [32] Yang, H. et al. TRH analogue microinjected into specific medullary nuclei stimulates gastric serotonin secretion in rats. Am. J. Physiol. 262, G216–G222 (1992).
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, secretion of antimicrobial peptides, such as defensins, by Paneth cells has an important role in host defense mechanisms against inflammatory and infectious diseases of the gut.29”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS modulation of gut–microbe signaling
What the sources say
- Not checked yetcites [29] Salzman, N. H., Underwood, M. A. & Bevins, C. L. Paneth cells, defensins, and the commensal microbiota: a hypothesis on intimate interplay at the intestinal mucosa. Semin. Immunol. 19, 70–83 (2007). source
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In the paper
“For example, Bifidobacterium bifidum and Lactobacillus acidophilus are able to promote motility, while Escherichia species can inhibit it.6”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Bidirectional signaling
What the sources say
- Not checked yetcites [6] Mazmanian, S. K. et al. A microbial symbiosis factor prevents intestinal inflammatory disease. Nature 453, 620–625 (2008). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Several signaling molecules used by the host for neuronal and neuroendocrine signaling (for example, catecholamines, serotonin, dynorphin, and cytokines) are also likely to be secreted into the gut lumen by neurons, immune cells and enterochromaffin cells, and the CNS is likely to have an important role in the release of these molecules.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS modulation of gut–microbe signaling
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In the paper
“Similarly to eukaryotes, prokaryotes communicate with each other through hormones and hormone-like compounds. This pattern of mutual bacterial inter action is called quorum sensing.41”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Bidirectional signaling
What the sources say
- Not checked yetcites [41] Nealson, K. H., Platt, T. & Hastings, J. W. Cellular control of the synthesis and activity of the bacterial luminescent system. J. Bacteriol. 104, 313–322 (1970). source
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In the paper
“Autoinducer 3 binds to the bacterial membrane receptor QseC, which results in its autophosphorylation. QseC then phosphorylates its response regulator, QseB, to initiate a complex signaling cascade that activates the expression of bacterial genes associated with virulence and motility, including the gene that presides over flagellum development.34”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Bidirectional signaling
What the sources say
- Not checked yetcites [34] Hughes, D. T. & Sperandio, V. Inter-kingdom signalling: communication between bacteria and their hosts. Nat. Rev. Microbiol. 6, 111–120 (2008). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Stress-induced changes in permeability involve activation of glial and mast cells in the gut, overproduction of interferon-γ and changes in the morphology of the colonic epithelium via reduced expression of tight junction protein 2 (zona occludens 2) and by occlusion of important components of the intestinal tight junction.28”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS-related changes in gut environment
What the sources say
- Not checked yetcites [28] Demaude, J. et al. Phenotypic changes in colonocytes following acute stress or activation of mast cells in mice: implications for delayed epithelial barrier dysfunction. Gut 55, 655–661 (2006). source
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In the paper
“In vitro norepinephrine stimulates the growth of several strains of enteric pathogens (reviewed elsewhere34) and magnifies the virulent properties of Campylobacter jejuni.36”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > CNS modulation of gut–microbe signaling
What the sources say
- Not checked yetcites [34] Hughes, D. T. & Sperandio, V. Inter-kingdom signalling: communication between bacteria and their hosts. Nat. Rev. Microbiol. 6, 111–120 (2008). source
- Not checked yetcites [36] Cogan, T. A. et al. Norepinephrine increases the pathogenic potential of Campylobacter jejuni. Gut 56, 1060–1065 (2007). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, autoinducer 3 can stimulate nor epinephrine receptors on the surface of eukaryotic cells, and α-2 receptors are present on the brush border of human enterocytes.51”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Microbe–gut–brain signaling
What the sources say
- Not checked yetcites [51] Valet, P. et al. Characterization and distribution of alpha 2-adrenergic receptors in the human intestinal mucosa. J. Clin. Invest. 91, 2049–2055 (1993). source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the effects of enteric microbiota to host signaling on various gut functions, including motility, secretion and immune function, have been studied extensively in healthy and diseased states, the possible effect of such microbial signaling beyond the gastro intestinal tract and on the nervous system has received little attention.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Microbe–gut–brain signaling
hedged- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbial signaling molecules could interact directly with afferent nerve terminals in situations where intestinal permeability is enhanced (for example, during inflammation or stress) or their signal could be relayed to neurons within the intestinal wall by ‘transducer cells’ in the epithelium.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Microbe–gut–brain signaling
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Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“That signaling molecules are released by the host into the lumen of the gastrointestinal tract during stress and that receptors and intercellular signaling mechanisms for these same molecules are present on certain luminal microbes34 strongly suggests that the nervous system can also directly modulate microbial behavior.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Bidirectional signaling
What the sources say
- Not checked yetcites [34] Hughes, D. T. & Sperandio, V. Inter-kingdom signalling: communication between bacteria and their hosts. Nat. Rev. Microbiol. 6, 111–120 (2008). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Enterochromaffin cells are distributed throughout the intestinal tract,52 and, like intestinal epithelial cells, those located in the intestinal mucosa are accessible to the enteric microbiota on the intestinal lumen side, and are in contact with afferent and efferent nerve terminals located on the lamina propria.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
What the sources say
- Not checked yetcites [52] Walsh, J. H. & Mayer, E. A. Gastrointestinal peptide hormones and signal transduction. In Gastrointestinal Disease: Pathophysiology, Diagnosis, Management 5th edn (Eds Sleizenger, M. & Fordtran, J.) 18–44 (WB Saunders, Philadelphia, 1993).
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similar mechanisms could have a role in the patho physiology of alterations in bowel habits for patients with IBS.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Microbe–gut–brain signaling
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, whereas the bacterial adrenergic agonist autoinducer 3 may mediate inhibition of intestinal fluid secretion—and thus delay transit rate—by binding to α-2 receptors on epithelial cells, other microbial factors may stimulate serotonin release by enterochromaffin cells to enhance fluid secretion, and thus accelerate transit rate.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This increase in luminal fluid in turn stimulates bowel motility, which ultimately helps remove intestinal contents, including pathogenic bacteria.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Interestingly, olfactory and taste receptors are expressed in enterochromaffin cells, and odorants present in the luminal environment (probably produced by the enteric microbiota) are also able to effect serotonin release by these cells.53”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
What the sources say
- Not checked yetcites [53] Braun, T., Voland, P., Kunz, L., Prinz, C. & Gratzl, M. Enterochromaffin cells of the human gut: sensors for spices and odorants. Gastroenterology 132, 1890–1901 (2007). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Nerve terminals of vagal afferents are located in close proximity to enterochromaffin cells, and these terminals express the serotonin-specific receptor 5-HT3R.67”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Vagal transmission of luminal signals
What the sources say
- Not checked yetcites [67] Raybould, H. E., Cooke, H. J. & Christofi, F. L. Sensory mechanisms: transmitters, modulators and reflexes. Neurogastroenterol. Motil. 16 (Suppl. 1), 60–63 (2004). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“A mechanism of this type might explain the reported upregulation of mucosal serotonin in a mouse model of postinfectious bowel dysfunction.66”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
What the sources say
- Not checked yetcites [66] Wheatcroft, J. et al. Enterochromaffin cell hyperplasia and decreased serotonin transporter in a mouse model of postinfectious bowel dysfunction. Neurogastroenterol. Motil. 17, 863–870 (2005). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The cholera toxin, a secretory enterotoxin from Vibrio cholerae, is known to trigger intestinal-fluid secretion by binding to the GM1 ganglioside on the surface of enterochromaffin cells. This interaction results in serotonin-mediated activation of secretomotor reflexes.61”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
What the sources say
- Not checked yetcites [61] Lencer, W. I. Microbes and microbial toxins: paradigms for microbial-mucosal toxins. V. Cholera: invasion of the intestinal epithelial barrier by a stably folded protein toxin. Am. J. Physiol. Gastrointest. Liver Physiol. 280, G781–G786 (2001). source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Inflammation-induced upregulation of serotonin signaling persists after the inflammation has receded, and, in this post inflammatory, upregulated state, microbe to entero chromaffin cell signaling may result in persistent symptoms of bowel dysfunction in human, post infectious IBS.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enterochromaffin cells as signal transducers
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The influence on the brain of stimuli such as cytokines and vagal signaling has been well characterized in animal models of inflammation, and the constellation of psychological symptoms associated with inflammation (fatigue, social withdrawal and loss of appetite) has been labeled the sickness behavior syndrome.72”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enteric microbiota and homeostatic functions
What the sources say
- Not checked yetcites [72] Watkins, L. R. & Maier, S. F. The pain of being sick: implications of immune-to-brain communication for understanding pain. Annu. Rev. Psychol. 51, 29–57 (2000). source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“As afferent nerves are not exposed to the luminal side of the intestine, under normal circumstances sensory neurons are indirectly activated by stimuli in the intestinal lumen via paracrine signaling, which is mediated by compounds such as serotonin, cholecystokinin, histamine, secretin, somatostatin, melatonin, uroguanylin, and corticotrophin-releasing factor, all of which can be released from ne”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Vagal transmission of luminal signals
What the sources say
- Not checked yetcites [68] Schonhoff, S. E., Giel-Moloney, M. & Leiter, A. B. Minireview: development and differentiation of gut endocrine cells. Endocrinology 145, 2639–2644 (2004). source
- Not checked yetcites [69] O'Hara, J. R., Ho, W., Linden, D. R., Mawe, G. M. & Sharkey, K. A. Enteroendocrine cells and 5-HT availability are altered in mucosa of guinea pigs with TNBS ileitis. Am. J. Physiol. Gastrointest. Liver Physiol. 287, G998–G1007 (2004). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As discussed earlier, in the presence of increased intestinal permeability (caused, for instance, by stress or gut inflammation), access of various bacterial products and inflammatory mediators to nerve endings in the mucosa would be a plausible mechanism for microbe to brain communication.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enteric microbiota and homeostatic functions
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Possible mechanisms underlying such changes include effects secondary to the production of gas and short-chain fatty acids by enteric microbiota, and direct enteric microbiota to host signaling.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Clinical impact of bidirectional signaling
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
In the paper
“Evidence of activation of the afferent vagal system was reported, which suggests a possible vagus-mediated microbe to brain signaling pathway.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enteric microbiota and homeostatic functions
What the sources say
- Not checked yetcites [73] Lyte, M., Li, W., Opitz, N., Gaykema, R. P. & Goehler, L. E. Induction of anxiety-like behavior in mice during the initial stages of infection with the agent of murine colonic hyperplasia Citrobacter rodentium. Physiol. Behav. 89, 350–357 (2006). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, in healthy organisms, signaling via epithelial transducer cells, such as enterochromaffin cells, may be the predominant mechanism.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Enteric microbiota and homeostatic functions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“In postinfectious IBS, major psychological stress around the time of gastroenteritis, trait anxiety, as well as extended duration of the infection, have been identified as risk factors for the persistence of symptoms.81”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Clinical impact of bidirectional signaling
What the sources say
- Not checked yetcites [81] Gwee, K. A. et al. The role of psychological and biological factors in postinfective gut dysfunction. Gut 44, 400–406 (1999). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One way to explain this resilience would be to consider the epithelium-associated biofilm as a permanent bacterial reservoir whose presence allows prompt reconstitution of the physiological microbiota profile in the gut lumen following a decline in luminal microbiota.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Clinical impact of bidirectional signaling
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
- Rests on an assumption: The gastrointestinal system is surprisingly resilient to transient changes in enteric microbiota induced by antibiotic treatment, colonic lavage, or, possibly, by spikes in psychological stress.
In the paper
“This reduction in abdominal girth was associ ated with an acceleration of orocecal as well as colonic transit and with an overall improvement in symptoms.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Potential therapeutic implications
What the sources say
- Not checked yetcites [13] Agrawal, A. et al. Clinical trial: the effects of a fermented milk product containing Bifidobacterium lactis DN-173-010 on abdominal distension and gastrointestinal transit in irritable bowel syndrome with constipation. Aliment. Pharmacol. Ther. (In press).
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Inflammation-induced upregulation of the mucosal serotonin signaling system would be expected to enhance the ability of the enteric microbiota to modulate gut motility through activation of peristaltic and secretomotor reflexes.”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Clinical impact of bidirectional signaling
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Evidence suggests that modification of the enteric microbiota by administration of antibiotics, probiotic bacteria or prebiotic substances (for example, certain fibers or lactulose) are beneficial in the treatment of IBD14 and improve some symptoms of IBS.12”
§ Principles and clinical implications of the brain–gut–enteric microbiota axis > Potential therapeutic implications
What the sources say
- Not checked yetcites [14] Vanderpool, C., Yan, F. & Polk, D. B. Mechanisms of probiotic action: implications for therapeutic applications in inflammatory bowel diseases. Inflamm. Bowel Dis. 14, 1585–1596 (2008). source
- Not checked yetcites [12] Spiller, P. Review article: probiotics and prebiotics in irritable bowel syndrome (IBS). Aliment. Pharmacol. Ther. (2008).
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Little is known about the possible role of direct signaling by luminal microorganisms to the brain in healthy and diseased states.
“However, little is known about the possible role of direct signaling by luminal microorganisms to the brain in healthy and diseased states.”
The paper relies on this without support.
The gastrointestinal system is surprisingly resilient to transient changes in enteric microbiota induced by antibiotic treatment, colonic lavage, or, possibly, by spikes in psychological stress.
“Notably, despite the intriguing possibility of adverse clinical consequences of long-term functional disruption in the brain–gut–microbe axis, the gastro intestinal system is surprisingly resilient to transient changes in enteric microbiota induced by antibiotic treatment, colonic lavage, or, possibly, by spikes in psychological stress.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Microbes can communicate with each other via metabolites, similar to those recognized by host cells and can thereby interact with gut ANS synapses (Rhee et al., 2009).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Rhee et al., 2009
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The size and quality of the intestinal mucus layer is believed to be mediated by sympathetic innervation where mucosal immune system modulation (Elenkov et al., 2000) and microbial composition and behavior alterations (commensal and pathogenic) were seen (Macfarlane and Dillon, 2007;Rhee et al., 2009)”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Rhee et al., 2009
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The concept of the microbiota-gut-brain axis thus emerged (Cryan and O'Mahony, 2011;De Palma et al., 2014;Rhee et al., 2009) based upon the rich historical legacy of the illustrious scientific figures discussed above, amongst many others.”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Rhee et al., 2009
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Gut-brain communication can also be achieved through vagus nerve signaling (57).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [57]
In the citing paper
“By regulating gastrointestinal functions, e.g., motility, nutrient absorption, acid production and mucosal immunity, the brain shapes the gut habitat and therefore selects for a distinct microbial profile [62].”
In the citing paper
“There are evidence that the gut microbiota modulates the CNS via the ENS, the ANS, the HPA axis and vice versa [124,213]”
From Gut microbiota role in irritable bowel syndrome: New therapeutic strategies (2016) · cites this paper as [124]
In the citing paper
“Mounting evidence suggests that the gastrointestinal microbiota influences host behaviour via bi-directional communication through what has been coined the microbiota-gut-brain axis [17, 18, 20, 29, 50, 60, 71].”
From Distinct actions of the fermented beverage kefir on host behaviour, immunity and microbiome gut-brain modules in the mouse (2020) · cites this paper as [60]
In the citing paper
“It has been also lately recognized that the gut-brain interactions might be essentially influenced by the gut microbiota (Borre et al., 2014;Grenham et al., 2011;Rhee et al., 2009).”
From The Gut-Brain Axis in Parkinson’s Disease: Possibilities for Food-Based Therapies (2017) · cites this paper as Rhee et al., 2009
Citations
Cites
An obesity-associated gut microbiome with increased capacity for energy harvest
Turnbaugh, P. J., Ley, R. E., Mahowald, M. A., Magrini, V., Mardis, E. R., & Gordon, J. I. (2006) · Nature · doi:10.1038/nature05414 · Cited by 12,444
Turnbaugh, P. J., Ley, R. E., Hamady, M., Fraser-Liggett, C. M., Knight, R., & Gordon, J. I. (2007) · Nature · doi:10.1038/nature06244 · Cited by 6,091
Gut flora in health and disease
Guarner, F., & Malagelada, J. (2003) · The Lancet · doi:10.1016/s0140-6736(03)12489-0 · Cited by 3,480 · cited 1×
“Approximately 10 11 bacterial cells can be found per gram of colon contents”
Sudo, N., Chida, Y., Aiba, Y., Sonoda, J., Oyama, N., Yu, X., Kubo, C., & Koga, Y. (2004) · The Journal of Physiology · doi:10.1113/jphysiol.2004.063388 · Cited by 2,735 · cited 1×
“Inflammation-associated hyperalgesia induced by a variety of stimuli, including administration of proinflammatory cytokines, was less intense in germ-free mice than in conventional mice”
A microbial symbiosis factor prevents intestinal inflammatory disease
Mazmanian, S. K., Round, J. L., & Kasper, D. L. (2008) · Nature · doi:10.1038/nature07008 · Cited by 2,340 · cited 1×
“The human gut harbors 400–1,000 different bacterial species”
Elenkov, I. J., Wilder, R. L., Chrousos, G. P., & Vizi, E. S. (2000) · Pharmacological Reviews · doi:10.1016/s0031-6997(24)01470-4 · Cited by 2,252
Gershon, M. D., & Tack, J. (2007) · Gastroenterology · doi:10.1053/j.gastro.2006.11.002 · Cited by 1,563
O’Mahony, L., McCarthy, J., Kelly, P., Hurley, G., Luo, F., Chen, K., O’Sullivan, G. C., Kiely, B., Collins, J. K., Shanahan, F., et al. (2005) · Gastroenterology · doi:10.1053/j.gastro.2004.11.050 · Cited by 1,448
Cellular Control of the Synthesis and Activity of the Bacterial Luminescent System
Nealson, K. H., Platt, T., & Hastings, J. W. (1970) · Journal of Bacteriology · doi:10.1128/jb.104.1.313-322.1970 · Cited by 1,301 · cited 1×
“This pattern of mutual bacterial interaction is called quorum sensing”
Kassinen, A., Krogius-Kurikka, L., Mäkivuokko, H., Rinttilä, T., Paulin, L., Corander, J., Malinen, E., Apajalahti, J., & Palva, A. (2007) · Gastroenterology · doi:10.1053/j.gastro.2007.04.005 · Cited by 1,002 · cited 1×
“A departure from the physiological balance of the enteric microbiota has been suggested as a factor in the pathophysiology of IBS, a condition in which abnormal gastrointestinal motility and secretion is implicated as a cause of alterations in bowel habits”
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Cited by
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Items 801–900 of 999
The Potential Impact of Selected Bacterial Strains on the Stress Response
Anker-Ladefoged, C., Langkamp, T., & Mueller‐Alcazar, A. (2021) · Healthcare · doi:10.3390/healthcare9050494 · Cited by 12
“This change leads to the death of some and the proliferation of other bacterial cultures, which in turn has effects on the stress response [12,13].”
BackgroundResultNamakin, K., Moghaddam, M. H., Sadeghzadeh, S., Mehranpour, M., Vakili, K. G., Fathi, M., Golshan-Tafti, A., Bayat, A., Tajik, A. H., Eskandari, N., et al. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01187-6 · Cited by 11
Liang, J., Li, X., Mao, C., Qin, Z., & Wang, R. (2025) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2025.102588 · Cited by 11
Huang, X., Lai, S., Lü, X., Wang, Y., Zhang, Y., Chen, G., Chen, P., Ye, K., Duan, M., Song, K., et al. (2022) · Journal of Affective Disorders · doi:10.1016/j.jad.2022.10.036 · Cited by 10
Huang, M., Liu, Y., Duan, R., Yin, J., & Cao, S. (2023) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2023.133267 · Cited by 10
Wei, J.-Q., Bai, J., Zhou, C., Yu, H., Zhang, W., Xue, F., & He, H. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e30014 · Cited by 11
“It is well known that the brain can modulate the enteric nervous system and gastrointestinal tract via the HPA axis and autonomic nervous system [47], and thus influence the gut microbiota by affecting the microenvironment [48].”
BackgroundNurturing development: how a mother's nutrition shapes offspring's brain through the gut
Ionescu, M.-I., Zahiu, C. D. M., Vlad, A., Galoş, F., Pîrcălăbioru, G. G., Zăgrean, A., & O’Mahony, S. M. (2024) · Nutritional Neuroscience · doi:10.1080/1028415x.2024.2349336 · Cited by 11
“These elements communicate through diverse signaling molecules, including neurotransmitters, hormones, neuropeptides, and microbiome-derived metabolites [73].”
Flores, J., Antonio, J. M., Suntornsaratoon, P., Meadows, V., Bandyopadhyay, S., Han, J., Singh, R., Balasubramanian, I., Upadhyay, R., Liu, Y., et al. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.107614 · Cited by 11
Gut Microbiome in Impulsively Violent Female Convicts
Langmajerová, M., Ježková, J., Kreisinger, J., Semerád, J., Titov, I., Procházková, P., Cajthaml, T., Jiřička, V., Vevera, J., & Roubalová, R. (2024) · Neuropsychobiology · doi:10.1159/000542220 · Cited by 12
“We hypothesize that the link between high tryptophan levels in the gut and reduced levels of serotonin in the brain of violent individuals is via afferent vagal neurons that innervate enterochromaf fi n cells and provide a direct pathway to neuronal circuits [40].”
Small, S. L. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102632 · Cited by 10
“…pathogenesis (Braak et al., 2006; Cersosimo and Benarroch, 2008), with some dysfunction in the gut-brain axis leading to misfolding of α -synuclein in the ENS (Bu et al., 2016; Mayer et al., 2015; Rhee et al., 2009; Shannon et al., 2012), contributing to disease progression (Minato et al., 2017).”
Xu, C., Zhao, W.-X., Yu, S., Yun, Y., Ma, T., Fan, N., Song, J., Wang, J., & Zhang, Q. (2025) · World Journal of Psychiatry · doi:10.5498/wjp.v15.i3.102567 · Cited by 10
The anti-inflammation pharmacodynamics of lithium: Therapy of bipolar disorder
Zhou, Y., Zheng, W., Guo, F., Wu, S., & Zhong, C. (2025) · Journal of Psychopharmacology · doi:10.1177/02698811251326942 · Cited by 11
Celiac Disease Autoimmunity and Emotional and Behavioral Problems in Childhood
Wahab, R. J., Beth, S. A., Derks, I. P. M., Jansen, P. W., Moll, H. A., & Jong, J. C. K. (2019) · PEDIATRICS · doi:10.1542/peds.2018-3933 · Cited by 14
Sharkey, K. A., & Savidge, T. (2014) · Autonomic Neuroscience · doi:10.1016/j.autneu.2014.03.004 · Cited by 11
Leung, C. Y., Leung, G. M., & Schooling, C. M. (2017) · Scientific Reports · doi:10.1038/s41598-017-15810-x · Cited by 12
Gut microbiota analysis and its significance in vasovagal syncope in children
Bai, W., Chen, S. Y., Tang, C., Qi, J., Cui, Q., Xu, M., Du, J., & Jin, H. (2019) · Chinese Medical Journal · doi:10.1097/cm9.0000000000000086 · Cited by 10
Lee, H., Lee, S., Kim, S., Lee, J., Ha, J., Choi, Y., Oh, H., Kim, Y., Lee, Y., Lim, D., et al. (2020) · Foodborne Pathogens and Disease · doi:10.1089/fpd.2019.2677 · Cited by 10
Sometti, D., Ballan, C., Wang, H., Braun, C., & Enck, P. (2021) · Scientific Reports · doi:10.1038/s41598-021-83994-4 · Cited by 11
Probiotics for Mental Health: A Review of Recent Clinical Trials
Esquivel, M. K. (2021) · American Journal of Lifestyle Medicine · doi:10.1177/15598276211049178 · Cited by 10
Analysis methods for the gut microbiome in neuropsychiatric and neurodegenerative disorders
Song, J. G., Yu, M., Lee, B., Lee, J., Hwang, S.-H., Na, D., & Kim, H. W. (2022) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2022.02.024 · Cited by 10
“However, recent groundbreaking studies have indicated that microorganisms living in the gut could influence the development of brain disorders by changing metabolites and neurochemicals [1,2].”
BackgroundWebster, S. E., Vos, D. G., Rothstein, T. L., & Holodick, N. E. (2022) · Frontiers in Microbiomes · doi:10.3389/frmbi.2022.994464 · Cited by 10
“, 2017), and homeostasis of the gut-brain axis (Rhee et al., 2009; Cryan and O’Mahony, 2011; Lyte, 2013).”
BackgroundA colon-specific prodrug of metoclopramide ameliorates colitis in an experimental rat model
Yang, Y., Kim, W., Kim, D., Jeong, S., Yoo, J., & Jung, Y. (2018) · Drug Design Development and Therapy · doi:10.2147/dddt.s185257 · Cited by 10
“The ENS–CNS communication, described as the gut–brain axis, plays an important role in the physiology of the GI tract, and a dysfunction of this axis causes disorders of the GI system.(3,4) Stresses of different origins alter the functioning of the gut–brain axis and are associated with GI disorders, including inflamm…”
BackgroundRole of gut microbiota in the GBR12909 model of mania-like behavior in mice
de Miranda, A. S., Vieira, É. L. M., Bastos, J. D. R., Ferreira, R. N., Nicoli, J. R., Teixeira, M. M., Vieira, L. Q., Moreira, F. A., & Teixeira, A. L. (2020) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2020.577292 · Cited by 10
Gut microbiota in anxiety and depression: Pathogenesis and therapeutics
Bibbò, S., Fusco, S., Ianiro, G., Settanni, C. R., Ferrarese, D., Grassi, C., Cammarota, G., & Gasbarrini, A. (2022) · Frontiers in Gastroenterology · doi:10.3389/fgstr.2022.1019578 · Cited by 13
“Moreover, the high prevalence of stress-related psychiatric symptoms in patients with gastrointestinal disorders supports the link between gut microbiota changes and psychiatric disorders (9).”
BackgroundPrebiotics and probiotics and Parkinson's disease
Amani, R., & Mehrabani, S. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-90052-2.00034-2 · Cited by 9
Zhang, W., Wang, X., Yin, S., Wang, Y., Li, Y., & Ding, Y. (2024) · European Journal of Nutrition · doi:10.1007/s00394-024-03401-2 · Cited by 9
“Therefore, the concept of “brain-gut-gut microbiota axis” appears, and the three jointly affect gastrointestinal health [10].”
The Interplay of Gut Microbiome in Health and Diseases
Mishra, T. K., Mallik, B., Kesheri, M., & Kanchan, S. (2024) · Springer eBooks · doi:10.1007/978-981-97-1769-9_1 · Cited by 10
Shen, C., Deshmukh, H., Santos, J. M., Elmassry, M. M., Presto, P., Driver, Z., Bhakta, V., Yakhnitsa, V., Kiritoshi, T., Ji, G., et al. (2024) · The Journal of Frailty & Aging · doi:10.14283/jfa.2024.65 · Cited by 9
“The brain can influence intestinal functions and gut microbial composition via the autonomic nervous system and the hypothalamic-pituitary-adrenal axis (3).”
Fritz, J., Lamadrid‐Figueroa, H., Muñoz-Rocha, T. V., Huerta-García, Y., Martínez-Silva, G., Valdivia, B. T., Martínez-Medina, S., Hernández-Chávez, C., Osorio-Valencia, E., Burris, H. H., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-73914-7 · Cited by 10
Advances in Gold Nanoparticles for the Diagnosis and Management of Alzheimer’s Disease
Sivamaruthi, B. S., Kesika, P., Sisubalan, N., & Chaiyasut, C. (2025) · Pharmaceutics · doi:10.3390/pharmaceutics17091158 · Cited by 9
“Molecular investigations have revealed a sophisticated interaction system that facilitates optimal gastrointestinal balance [61].”
Yang, L., Fan, S., Sun, L., Han, J., Wang, M., & Yu, T. (2025) · Frontiers in Neurology · doi:10.3389/fneur.2025.1643305 · Cited by 9
Influence of Gut Microbes on the Brain-Gut Axis (Gut 2011;60:307-317)
Lee, Y. Y., & Chua, A. S. B. (2011) · Journal of Neurogastroenterology and Motility · doi:10.5056/jnm.2011.17.4.427 · Cited by 9
“Psychological stress and its morbidity are often encountered in functional gut disorders and this emphasizes the importance of the brain-gut axis in regulating gastrointestinal physiology.(1,2) The bidirectional interaction between the gut and the brain is vital in maintaining homeostasis but the exact mechanism on how”
BackgroundRao, X., Liu, L., Wang, H., Yu, Y., Li, W., Chai, T., Zhou, W., Ji, P., Song, J., Wei, H., et al. (2021) · Experimental Neurobiology · doi:10.5607/en20055 · Cited by 10
“Moreover, accumulating studies have revealed bidirectional communication between the gut microbiota and the brain, and have proposed a novel conceptual model of a “microbiota–gut–brain axis” [3-5].”
BackgroundTamada, H., Ikuta, K., Makino, Y., Joho, D., Suzuki, T., Kakeyama, M., & Matsumoto, M. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.882339 · Cited by 9
Mittinty, M. M., Lee, J., Walton, D. M., El-Omar, E. M., & Elliott, J. M. (2022) · Pathogens · doi:10.3390/pathogens11070716 · Cited by 9
Darmmikrobiom und Psyche: der Paradigmenwechsel im Konzept der Hirn-Darm-Achse
Konturek, P. C., & Zopf, Y. (2016) · MMW - Fortschritte der Medizin · doi:10.1007/s15006-016-8304-z · Cited by 9
Depletion of stercobilin in fecal matter from a mouse model of autism spectrum disorders
Sekera, E. R., Rudolph, H. L., Carro, S. D., Morales, M. J., Bett, G. C. L., Rasmusson, R. L., & Wood, T. D. (2017) · Metabolomics · doi:10.1007/s11306-017-1277-9 · Cited by 9
“It is known that the microbiome of the gut regulates the homeostasis of the central nervous system (Rhee et al. 2009; Sherwin et al. 2016).”
Stool consistency is significantly associated with pain perception
Shiro, Y., Arai, Y.-C. P., Ikemoto, T., & Hayashi, K. (2017) · PLoS ONE · doi:10.1371/journal.pone.0182859 · Cited by 11
İnsan Mikrobiyomu: Beslenme ve Sağlık Üzerindeki Etkileri
Cetinbas, S., Kemeriz, F., Göker, G., Biçer, İ., & Velioğlu, Y. S. (2017) · Akademik Gıda · doi:10.24323/akademik-gida.370267 · Cited by 9
“Enterik mikrobiyomların bağırsak beyin iletişimi üzerindeki aşamalarının enterik mikrobiyotayı fazlasıyla etkilediğini göstermektedir [19].”
Bai, J., Wei, J.-Q., Tian, Q., Xue, F., Zhang, W., & He, H. (2023) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2023.1292835 · Cited by 9
“At the same time, the brain has the capacity to regulate the gastrointestinal tract and the enteric nervous system, thereby exerting an influence on the composition of the gut microbiota (Rhee et al., 2009).”
BackgroundGut microbiota: the indispensable player in neurodegenerative diseases
Li, S., Cai, Y., Wang, S., Luo, L., Zhang, Y., Huang, K., & Guan, X. (2024) · Journal of the Science of Food and Agriculture · doi:10.1002/jsfa.13509 · Cited by 11
Gut-brain axis and neuroplasticity in health and disease: a systematic review
Napoli, A. D., Pasquini, L., Visconti, E., Vaccaro, M., Rossi‐Espagnet, M. C., & Napolitano, A. (2024) · La radiologia medica · doi:10.1007/s11547-024-01938-0 · Cited by 9
“The human gut is a large organ and represents a major surface for microbial colonization, harboring 400–1,000 different bacterial species, which make up an intricate network of cohabiting organisms [4].”
InfluentialZhu, H., He, H., Yang, M., Zhu, H., Hagiwara, A., Shu, L., Xu, J., Miao, Y., Han, X., & Wang, C. (2025) · iScience · doi:10.1016/j.isci.2025.114044 · Cited by 8
Gut microbial metabolism via hippocampal indole-AhR signaling regulates emotional symptoms
Wang, T.-T., Luo, Y.-J., Feng, W., Jiang, L., Yu, Q.-S., He, Y.-T., Guan, L., Zhu, B.-Q., Jiang, H., Li, M., et al. (2026) · Cell Metabolism · doi:10.1016/j.cmet.2026.03.003 · Cited by 8
Li, J., Yu, H., Wang, Y., Wang, B., Zhang, R., Chen, S., & Duan, G. (2022) · Journal of Public Health · doi:10.1093/pubmed/fdac078 · Cited by 8
Mullaney, J. A., Roy, N. C., Halliday, C., Young, W., Altermann, E., Kruger, M. C., Dilger, R. N., & McNabb, W. C. (2022) · Frontiers in Microbiology · doi:10.3389/fmicb.2022.960492 · Cited by 11
Understanding the potential causes of gastrointestinal dysfunctions in multiple system atrophy
Craig, C. F., Finkelstein, D. I., McQuade, R. M., & Diwakarla, S. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106296 · Cited by 8
Lu, T., Huang, C., Weng, R., Wang, Z., Sun, H., & Ma, X. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e24899 · Cited by 9
“The intestinal microbiota can regulate the nutrient supply [34], prevent pathogen colonisation, and shape and maintaining host immunity [35].”
BackgroundGastrointestinal microbiology in autistic spectrum disorder: a review
Gondalia, S. V., Palombo, E. A., Knowles, S. R., & Austin, D. (2010) · Reviews in Medical Microbiology · doi:10.1097/mrm.0b013e32833a3dc9 · Cited by 8
“cine-phenylalanine), are able to stimulate the enteric nervous system and influence the rate of gut transit [21].”
BackgroundKumar, V., Thakur, A. K., Verma, S., Yadav, V., & Chatterjee, S. S. (2015) · TANG [HUMANITAS MEDICINE] · doi:10.5667/tang.2014.0026 · Cited by 8
Rationale for Investigating Stool Metabolites and Microbiota in Women With Fecal Incontinence
Arya, L. A. (2017) · Diseases of the Colon & Rectum · doi:10.1097/dcr.0000000000000751 · Cited by 8
Immune-microbiome interplay and its implications in neurodegenerative disorders
Uniyal, A., Tiwari, V., Rani, M., & Tiwari, V. (2021) · Metabolic Brain Disease · doi:10.1007/s11011-021-00807-3 · Cited by 9
“The three major peripheral components of GBA are the sympathetic nervous system (SNS), autonomic nervous system (ANS) and hypothalamic-pituitary-axis (HPA) (Rhee et al. 2009).”
BackgroundHull, R., Lolas, G., Makrogkikas, S., Jensen, L. D., Syrigos, K. N., Evangelou, G., Padayachy, L. C., Egbor, C., Mehrotra, R., Makhafola, T. J., et al. (2021) · Microorganisms · doi:10.3390/microorganisms9102129 · Cited by 8
“This bidirectional interaction has been dubbed the gut–brain axis [28,29].”
BackgroundThe impact of the Th17:Treg axis on the IgA-Biome across the glycemic spectrum
Essigmann, H. T., Hoffman, K. L., Petrosino, J. F., Jun, G., Aguilar, D. A., Hanis, C. L., DuPont, H. L., & Brown, E. L. (2021) · PLoS ONE · doi:10.1371/journal.pone.0258812 · Cited by 8
Gut microbiome and neurosurgery: Implications for treatment
Willman, J., Willman, M., Reddy, R., Fusco, A. F., Sriram, S., Mehkri, Y., Charles, J. H., Goeckeritz, J., & Lucke-Wold, B. P. (2022) · Clinical and Translational Discovery · doi:10.1002/ctd2.139 · Cited by 9
Linsalata, M., Prospero, L., Riezzo, G., Orlando, A., D’Attoma, B., Ignazzi, A., & Russo, F. (2022) · Neurogastroenterology & Motility · doi:10.1111/nmo.14512 · Cited by 7
A New Insight on Feasibility of Pre-, Pro-, and Synbiotics-based Therapies in Alzheimer’s Disease
Talebi, M., Ebrahimi, V., Rasouli, A., Farjami, A., Soofiyani, S. R., Soleimanian, A., Forouhandeh, H., & Tarhriz, V. (2022) · Journal of Reports in Pharmaceutical Sciences · doi:10.4103/jrptps.jrptps_170_21 · Cited by 8
Emerging and Evolving Topics in Multiple Sclerosis Pathogenesis and Treatments
Flamme, A. C. L., & Orian, J. M. (2015) · Current topics in behavioral neurosciences · doi:10.1007/978-3-319-25543-9 · Cited by 7
Stroke-Associated Pneumonia and the Brain-Gut-Lung Axis
Bai, J., Zhao, Y., Wang, Z., Qin, P., Huang, J., Cheng, Y., Wang, C., Chen, Y., Liu, L., Zhang, Y., et al. (2025) · The Neurologist · doi:10.1097/nrl.0000000000000626 · Cited by 8
Varnas, D., Kunevičius, A., Burokas, A., & Urbonas, V. (2025) · Medicina · doi:10.3390/medicina62010065 · Cited by 7
“While the concept of the gut microbiota and brain connection was longstanding [29], one of the earliest mentions of the term “gut–brain axis” (GBA) is in a 2011 study by Grenham et al., in which the authors explored the complex bidirectional communication network between the central nervous system…”
Diet and gut microbiota during depression and stress
Khazaei, M., Bahar, A., Arabestani, M. R., & Tahmasebi, H. (2026) · Discover Food · doi:10.1007/s44187-026-00846-8 · Cited by 8
“The brain-gut-microbiota axis may include the parasympathetic and sympathetic autonomic nervous systems, the neuroimmune systems, the intestinal microbiota, the CNS neuro-endocrine system, and the ENS [42, 43].”
Wu, Y., Liu, S., Dong, H., Zhang, J., Lu, R., Yang, Q., Jaman, R., Zhu, J., Zhang, C., & Zhou, J. (2026) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2026.119810 · Cited by 8
Gut Microbiota Dysbiosis and COVID-19: Possible Links
Aktaş, B. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819265-8.00072-3 · Cited by 7
Microbiota and nutrition as risk and resiliency factors following prenatal alcohol exposure
Upreti, D., Rouzer, S. K., Bowring, A., Labbe, E., Kumar, R. P., Miranda, R. C., & Mahnke, A. H. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1182635 · Cited by 7
“Reciprocally, gut microbiota can shape human health through the production and release of metabolites into human circulation, impacting metabolic, immune, and neuroendocrine networks (Rhee et al., 2009).”
BackgroundThe gut microbiota-neuroimmune crosstalk and neuropathic pain: a scoping review
Nawarathna, G. S., Fakhruddin, K. S., Shorbagi, A., & Samaranayake, L. P. (2023) · Gut Microbiome · doi:10.1017/gmb.2023.7 · Cited by 7
“Similarly, nerve injury could impact gut microbial composition via alterations in gut functionality, such as the release of neurotransmitters, motility, and intestinal immune tone (Rhee et al., 2009).”
BackgroundCrosstalk between COVID-19 and the gut-brain axis: a gut feeling
Kalam, N., & Balasubramaniam, V. R. M. T. (2024) · Postgraduate Medical Journal · doi:10.1093/postmj/qgae030 · Cited by 8
Ding, R., Lu, J., Huang, X., Deng, M., Wei, H., Jiang, G., Zhu, H., & Yuan, H. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.113100 · Cited by 8
Meanings, measurements, and musings on the significance of patterns in human microbiome variation
Schnorr, S. L. (2018) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2018.06.014 · Cited by 8
Microbiome and Schizophrenia: Current Evidence and Future Challenges
Cordeiro, T. M. E., Zhang, X., Graubics, K., Colwell, R. R., & Teixeira, A. L. (2020) · Current Behavioral Neuroscience Reports · doi:10.1007/s40473-020-00206-5 · Cited by 7
Tryptophan Metabolism and the Microbiome-Gut-Brain Axis
Clarke, G. A., Villalobos-Manríquez, F., & Marin, D. C. (2021) · Oxford University Press eBooks · doi:10.1093/oxfordhb/9780190931544.013.13 · Cited by 7
Selim, A., Salem, S. S., Albasher, N., Bakrmom, G., Al-Anzi, S. K., & Jradi, H. (2021) · Clinical Nursing Research · doi:10.1177/10547738211020437 · Cited by 8
“Psychological stress has a significant impact on the gut in terms of intestinal sensitivity, motility, secretion, and permeability (Rhee et al., 2009).”
BackgroundБелкина, Т. В., Averina, O. V., Savenkova, E. V., & Даниленко, В. Н. (2021) · Biology Bulletin Reviews · doi:10.1134/s2079086421040034 · Cited by 7
“…of interest in the bacteria inhabiting the human gastrointestinal tract (microbiota) manifested itself 10–15 years ago, after the fact of bidirectional gut–brain communication had been established (Rhee et al., 2009; Foster and Neufeld, 2013; Averina and Danilenko, 2017; Cryan et al., 2019).”
BackgroundRéus, G. Z., Manosso, L. M., Arent, C. O., Borba, L. A., & Abelaira, H. M. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1570159x20666220329143804 · Cited by 7
Huang, J., Chen, T., Zhang, J., Ma, X., Wang, F., & Tang, X. (2023) · The American Journal of Chinese Medicine · doi:10.1142/s0192415x23500398 · Cited by 7
IgA-Biome Profiles Correlate with Clinical Parkinson’s Disease Subtypes
Brown, E. L., Essigmann, H. T., Hoffman, K. L., Alexander, A. S., Newmark, M. E., Jiang, Z., Suescun, J., Schiess, M. C., Hanis, C. L., & DuPont, H. L. (2023) · Journal of Parkinson s Disease · doi:10.3233/jpd-230066 · Cited by 7
“…gut microbiome occur prior to the manifestation of any overt Parkinson’s disease symptoms, suggesting that Parkinson’s disease etiology and disease subtype presentation may be intimately linked to the architecture of the gut microbiome by impacting the gut-brain-enteric microbiota axis [2, 12, 13].”
The Human Gut Microbiome and Its Role in Obesity and the Metabolic Syndrome
Mullin, G. E., & Delzenne, N. M. (2014) · Springer eBooks · doi:10.1007/978-1-4939-0548-5_7 · Cited by 7
Can Intestinal Constipation Be Modulated by Prebiotics, Probiotics and Symbiotics?
Sant’Anna, M. D. S. L., & Ferreira, C. L. D. L. F. (2014) · Food and Nutrition Sciences · doi:10.4236/fns.2014.512120 · Cited by 7
“Therefore, the disturbance of the microbiota balance may predispose the host to change the motility, resulting in diarrhea, common in irritable bowel syndrome, or constipation [25].”
BackgroundENVOLVIMENTO DA FLORA INTESTINAL NA MODULAÇÃO DE DOENÇAS PSIQUIÁTRICAS
Lach, G., Morais, L. H., Costa, A. P., & Hoeller, A. A. (2017) · VITTALLE - Revista de Ciências da Saúde · doi:10.14295/vittalle.v29i1.6413 · Cited by 12
“Desde o século XIX especula-se o impacto recíproco do trato GI no encéfalo, mas somente nas últimas décadas uma rota bidirecional de comunicação entre estes sistemas, posteriormente denominados eixo encéfalo-intestinal, tornou-se reconhecido (44,45).”
BackgroundRole of Microbiota in Neurodegenerative Diseases
Sobol, C. V. (2018) · Russian Journal of Developmental Biology · doi:10.1134/s1062360418060061 · Cited by 7
“The violation of such gut–brain interaction can be observed in different types of GI and CNS, diseases (Rhee et al., 2009; Lyte and Cryan, 2014; Mayer et al., 2015).”
BackgroundImpact of Integrated Care in a Pediatric Gastroenterology Clinic on Psychology Utilization
Lamparyk, K., Debeljak, A., Aylward, L., & Mahajan, L. A. (2018) · Clinical Practice in Pediatric Psychology · doi:10.1037/cpp0000218 · Cited by 7
Microbiota-Gut-Brain Axis, Part 1
Ross, S. M. (2017) · Holistic Nursing Practice · doi:10.1097/hnp.0000000000000203 · Cited by 7
Neurohormonal signalling in the gastrointestinal tract: new frontiers
Sharkey, K. A., & Mawe, G. M. (2014) · The Journal of Physiology · doi:10.1113/jphysiol.2014.275487 · Cited by 7
“…has expanded even further with the recognition of the importance of the gut microbiota in digestive system physiology and in gut–brain communication, extending the notion of the gut–brain axis to that of the microbiota–gut–brain axis (Rhee et al. 2009; Bercik et al. 2012; Mayer et al. 2014).”
BackgroundPolic, I. I. (2018) · Cited by 7
Kalaga, P., & Ray, S. K. (2025) · Brain Sciences · doi:10.3390/brainsci15020197 · Cited by 6
“All these three Changes to this line of communication have a direct impact on the size and quality of the mucosa, where most of the GI-based bacteria live [27]. genera engage in the production of useful SCFAs.”
Using synthetic biology to understand the gut-brain axis
Cesaro, A., Broset, E., Salimando, G. J., Öztekin, S., Mai, D., Bennett, M. L., & de la Fuente‐Núñez, C. (2025) · Cell Reports Physical Science · doi:10.1016/j.xcrp.2025.102458 · Cited by 7
Deciphering T Cell Dynamics in Alzheimer's Disease Pathogenesis: Insights and Implications
Yang, Q., Qiu, Y., Ni, J., Li, H., & Qing, H. (2025) · Current Neuropharmacology · doi:10.2174/011570159x350611250303044527 · Cited by 7
Li, Q., Zhang, Y., Wang, X., Dai, L., & Zhao, W. (2025) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2025.1444793 · Cited by 7
Nieto‐Fabregat, F., Mercogliano, M., Cangiano, A., Vitiello, G., Andretta, E., Clifton, L. A., Vanacore, A., Buono, L., Campanero‐Rhodes, M. A., Solı́s, D., et al. (2025) · JACS Au · doi:10.1021/jacsau.5c00441 · Cited by 6
A closer look at the role of nutrition in children and adults with ADHD and neurodivergence
Hunter, C., Smith, C., Davies, E., Dyall, S. C., & Gow, R. V. (2025) · Frontiers in Nutrition · doi:10.3389/fnut.2025.1586925 · Cited by 9
“From this perspective, children with ADHD and (undiagnosed) food intolerances may crave the very foods they are in fact intolerant to reflecting a type of microbial manipulation (154–156).”
Chang, J. Y., Jung, H., Moon, C. M., Kim, S., Shim, K., Jung, S.-A., & Min, S. K. (2023) · Frontiers in Medicine · doi:10.3389/fmed.2023.1248465 · Cited by 6
“…intricate interactions among gastrointestinal (GI) motor dysfunction (3), visceral hypersensitivity (4), infections (5), alteration of the gut microbiota (6), dysfunction of the brain-gut axis (1), psychosocial factors including early life events (7), abuse (8), and social behavioral learning (9).”
BackgroundMicrobiota gut-brain axis: implications for pediatric-onset leukodystrophies
Vaia, Y., Bruschi, F., Tagi, V. M., Tosi, M., Montanari, C., Zuccotti, G., Tonduti, D., & Verduci, E. (2024) · Frontiers in Nutrition · doi:10.3389/fnut.2024.1417981 · Cited by 9
“GM can influence the systemic health by contributing to the signaling along the GBA, whereas the Central Nervous System (CNS), Enteric Nervous System (ENS), neuroendocrine and neuroimmune pathways are all involved in the bidirectional communication between the CNS and the GI tract (35, 36).”
BackgroundFaysal, M. F., Zehravi, M., Amin, M. A., Rab, S. O., Jahnavi, P., Arjun, U. V. N. V., Gupta, J. K., Billah, A. A. M., Vodeti, R., Prasad, P. D., et al. (2025) · Pathology - Research and Practice · doi:10.1016/j.prp.2025.156090 · Cited by 6
Blagonravova, A. S., Zhilyaeva, T. V., & Kvashnina, D. V. (2021) · Journal of microbiology epidemiology immunobiology · doi:10.36233/0372-9311-83 · Cited by 6
Sathicq, M. B., Sbaffi, T., Borgomaneiro, G., Cesare, A. D., & Sabatino, R. (2021) · Journal of Limnology · doi:10.4081/jlimnol.2021.2054 · Cited by 6
Jang, H., Kim, S. Y., Kim, B. S., Kim, M., Jung, J., & Won, C. W. (2022) · Annals of Geriatric Medicine and Research · doi:10.4235/agmr.22.0092 · Cited by 6
Hamad, I., Broeckhoven, J. V., Cardilli, A., Hellings, N., Strowig, T., Lemmens, S., Hendrix, S., & Kleinewietfeld, M. (2023) · Nutrients · doi:10.3390/nu15194184 · Cited by 7
“Perturbations in the CNS lead to changes in the luminal/mucosal habitat of the gut, which in turn may affect microbial composition [7,8].”
BackgroundNaik, A., & Godbole, M. S. (2024) · Cancer Reports · doi:10.1002/cnr2.70005 · Cited by 6
“This affects the direct communication with the visceral afferent nerves and immune cells in the host [70].”
Wang, Y., Huang, H., Chiu, Y.-W., Chao, W., Chuang, T., Lu, Y.-C., & Lin, M. (2012) · Journal of Food and Drug Analysis · doi:10.6227/jfda.2012200312 · Cited by 6
Sadaqat, Z., Kaushik, S., & Kain, P. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.96503 · Cited by 11
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“In healthy subjects, the gut microbiome contributes to important physiological processes, such as protection against pathogens, activation of the immune system, digestion of food components and production of vitamins [6].”
Background
Metadata
- Authors
- Rhee, S. H., Pothoulakis, C., & Mayer, E. A.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Mayer, Emeran A.
- Venue
- Nature Reviews Gastroenterology & Hepatology
- Published
- 2009-05
- Volume
- 6
- Issue
- 5
- Pages
- 306-314
- ISSN
- 1759-5045 (ISSN-L)
- 1759-5053
- PMC
- PMC3817714
- OpenAlex
- W2076087096
- Semantic Scholar
- 8d46dbee61595ddb88b690b9979d376a39c691fe
- Cited by
- 1,342
- References
- 87
- Citations by year
- 2026: 66 · 2025: 107 · 2024: 112 · 2023: 130 · 2022: 122 · 2021: 127 · 2020: 114 · 2019: 90 · 2018: 84 · 2017: 94 · 2016: 77 · 2015: 48 · 2014: 55 · 2013: 45 · 2012: 33
- FWCI
- 1.81
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Nature Reviews Gastroenterology & Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK033506, P01 DK-33506, R01 DK072471, R01 DK 48351, R01DK048351, R01-DK47343, P50DK064539, P-50DK64539, R01DK047343, R01DK060729)
- National Center for Complementary and Integrative Health (R24AT002681)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Keywords
- gut-brain axis, gut microbiota, enteric microbiota, two-way communication, central nervous system, enterochromaffin cells, intestinal permeability, lamina propria, gastrointestinal motility, gastrointestinal secretion, functional bowel disorders, inflammatory bowel disease
- MeSH terms
- Brain, Humans, Intestines, Inflammatory Bowel Diseases, Enteric Nervous System
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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