Host microbiota constantly control maturation and function of microglia in the CNS
Open accessAbstract
As the tissue macrophages of the CNS, microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. We observed substantial contributions of the host microbiota to microglia homeostasis, as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype, leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulated microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings suggest that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be rectified to some extent by complex microbiota.
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Perturbations of the gut microbiota by antibiotics systemically produce altered immune responses in experimental models, notably toward a pro-inflammatory profile.
“perturbations of the gut microbiota by antibiotics systemically produce altered immune responses in experimental models, notably toward a pro-inflammatory profile (6).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [6]
The ‘Temporal depletion’ section reports that antibiotics depleted gut microbiota and altered microglia in mice. But the Discussion describes blunted early responses after microbial depletion, not a shift toward a pro-inflammatory profile; the reported effects concern CNS microglia rather than systemic immune responses. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredGerm-free animals display global deficiency in microglia and reduced genes needed to express type I interferon receptors such as Jak3 and Stat1.
“Erny et al. 147 illustrated that germ-free animals display global deficiency in microglia and the genes needed to express type I interferon receptors such as Janus kinase 3 (Jak3) and signal transducer and activator of transcription 1 (Stat1), were reduced.147”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [147]
In “Germ-free animals display global defects in microglia,” the paper reports reduced Jak3 and Stat1 expression in germ-free microglia and describes broad defects in their maturation and function. It does not report a global deficiency in microglial cell numbers: it found significantly more microglia in every brain region investigated. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe function of microglia can be restored by reconstruction of gut microbiota or their metabolites, indicating that microbiota may be involved in the activity of the innate immune system in the brain via microbial metabolites and intestinal secretions.
“The function of microglia can be restored by the reconstruction of gut microbiota or their metabolites, indicating that microbiota may also be involved in the activity of the innate immune system in the brain via microbial metabolites and intestinal secretions.147”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [147]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredSCFAs from intestinal microbiota are key molecules regulating the maturation, morphology and function of microglia.
“In addition, SCFAs from intestinal microbiota are key molecules regulating the maturation, morphology and function of microglia.147”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [147]
The Discussion reports that gut microbiota affect microglial maturation, shape and responses to pathogens. It mentions SCFAs only as metabolites that may enter circulation and could affect immune regulation and CNS function; it does not establish them as the key molecules regulating all three microglial features. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMicroorganisms influence the brain through their ability to produce and modify metabolic, immunological and neurochemical factors in the gut that ultimately impact the central nervous system.
“Microorganisms influence the brain through their ability to produce and modify metabolic, immunological and neurochemical factors in the gut that ultimately impact on the central nervous system59.”
From Association between attention-deficit/hyperactivity disorders and intestinal disorders: A systematic review and Meta-analysis (2025) · cites this paper as [59]
Microorganisms can influence central nervous system processes bidirectionally via the vagus nerve and through modulation of the immune system, the hypothalamic-pituitary-adrenal axis, tryptophan metabolism, neurotransmitter synthesis, and metabolites such as short-chain fatty acids that possess neuroactive properties.
“Microorganisms can influence CNS processes bidirectionally via the vagus nerve (12) and through modulation of the immune system (6), the hypothalamic-pituitary-adrenal (HPA) axis (13, 14), and tryptophan metabolism (15), along with their ability to synthetize a number of neurotransmitters (16–18) and produce metabolites, such as short-chain fatty acids (SCFAs), that possess neuroactive properties”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [6]
The influence of the gut microbiota is not restricted to the gastrointestinal tract; it plays a major role in bidirectional communication between the gastrointestinal tract and the central nervous system.
“it plays a major role in the bidirectional communication between the GI tract and the central nervous system (CNS).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [6]
Non-colonized young germ-free mice exhibit stunted microglia under homeostatic conditions, while microglia from specific-pathogen-free mice show normal maturation and function.
“While microglia from specific pathogen-free (SPF) mice shows normal maturation and function, non-colonized young GF mice exhibit stunted microglia under homeostatic conditions.”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [6]
The gut microbiota plays a pivotal role in the development and functionality of the immune system in the central nervous system.
“the gut microbiota seems to play a pivotal role in the development and functionality of the immune system in the CNS.”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [6]
Oral application of a mixture of the three major short-chain fatty acids acetate, propionate, and butyrate was sufficient to drive maturation of microglia in germ-free mice.
“the oral application of a mixture of the three major SCFAs acetate, propionate, and butyrate was sufficient to drive maturation of microglia in GF mice (6).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [6]
The ‘Germ-free animals display global defects in microglia’ section describes immature microglia in germ-free mice, while ‘Defective microglia can be restored by a complex microbiota’ describes restoration after recolonization. Searches for SCFAs, acetate, propionate, butyrate, and oral supplementation found no passage in our copy addressing whether the three-acid mixture drove maturation. (LLM, conf=0.73)
Experimental — accuracy not yet measuredThe microglial defects and immaturity were partially restored by recolonization with complex microbiota and SCFAs supplementation.
“However, the microglial defects and immaturity were partially restored by recolonization with complex microbiota and SCFAs supplementation.191”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [191]
Under homeostatic conditions, the gut microbiome is responsible for regulating microglial maturation and activation via short-chain fatty acids (SCFAs) release.
“Under homeostatic conditions, the gut microbiome is responsible for regulating microglial maturation and activation via short-chain fatty acids (SCFAs) release.190,191”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [191]
FFAR2-deficient SPF mice develop microglial defects resembling those in GF mice.
“It was reported that the FFAR2-deficient SPF mice developed microglial defects resembling GF mice.191”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [191]
The microbiota is essential for microglia maturation and function.
“Thus, the microbiota is essential for microglia maturation and function.”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [52]
Genes highly expressed in microglia during early developmental stages that promote cell proliferation and survival are aberrantly up-regulated in microglia isolated from adult GF mice.
“Concurrently, genes highly expressed in microglia during early developmental stages that promote cell proliferation and survival, including Csf1r and Ddit4, are aberrantly up-regulated in microglia isolated from adult GF mice.”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
The immature gene expression profile resulting from the absence of gut microbiota contributes to the inability of microglia to properly respond to immunostimulants such as LPS and lymphocytic choriomeningitis virus.
“The immature gene expression profile resulting from the absence of gut microbiota contributes to the inability of microglia to properly respond to immunostimulants such as LPS and the lymphocytic choriomeningitis virus, both of which failed to elicit an appropriate activation response in microglia from GF mice (Erny et al., 2015).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
Microglia from adult GF mice show distinct differences in density and morphology compared with those derived from SPF mice.
“Consistent with patterns observed prenatally, microglia from adult GF mice, lacking constant postnatal input from gut microbiota, show distinct differences in density and morphology compared with those derived from SPF mice (Erny et al., 2015).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
Microglial development appears arrested in GF mice, as supported by high expression of genes characteristic of early and premicroglia in microglia from adult GF mice.
“Microglial development appears arrested in GF mice, as supported by high expression of genes characteristic of early and premicroglia in microglia from adult GF mice.”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
Microglia from adult GF mice display differential expression of genes associated with microglial maturation, including down-regulation of genes that regulate cell activation and immune system defense pathways.
“Microglia from adult GF mice also display differential expression of genes associated with microglial maturation, including down-regulation of genes that regulate cell activation and immune system defense pathways, such as Mapk8, IL-1α, Ly86, Jak3, and Stat1, all of which are normally highly expressed in adult microglia (Fig. 1; Erny et al., 2015; Matcovitch-Natan et al., 2016).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
In SPF mice, a diverse gut microbiota promotes microglial development and maturation.
“In SPF mice, a diverse gut microbiota promotes microglial development and maturation.”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
Supplementation of drinking water with a mixture of three primary SCFAs (acetic acid, propionic acid, and butyric acid) rescued the immature genetic and morphological phenotype of microglia from GF mice.
“Supplementation of drinking water with a mixture of three primary SCFAs (acetic acid, propionic acid, and butyric acid) rescued the immature genetic and morphological phenotype of microglia from GF mice (Erny et al., 2015).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
SPF mice lacking the free fatty acid receptor 2 (FFAR2), a GPCR required for SCFA signaling in the gut, exhibited a microglial phenotype similar to that observed in GF mice.
“SPF mice lacking the free fatty acid receptor 2 (FFAR2), a GPCR required for SCFA signaling in the gut, exhibited a microglial phenotype similar to that observed in GF mice (Erny et al., 2015).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
Given the requirement for constant input from the gut microbiota for normal microglial development and function, it is plausible that microbial effects on neural development and behavior may occur through changes in microglial activity.
“Given the requirement for constant input from the gut microbiota for normal microglial development and function, it is plausible that microbial effects on neural development and behavior may occur through changes in microglial activity (Erny et al., 2015; Thion et al., 2018).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Erny et al., 2015
Eliminating gut microbiota changes microglial numbers, size, transcriptomes, and surveillance functions and lowers host-defense genes.
“Eradication of gut microbiota also alters microglial numbers, size, transcriptomes, and surveillance functions and downregulates host-defense genes147.”
From Microglia in neurodegeneration (2018) · cites this paper as [147]
Intestinal bacterial colonization controls immune system maturation and development in the CNS.
“Intestinal bacterial colonization regulates immune system maturation and development in the CNS.”
From Microglia in neurodegeneration (2018) · cites this paper as [147]
Recolonization with complex microbiota or microbiota-derived products partially restores microglial properties.
“Recolonization with a complex microbiota or with microbiota-derived products partially restores microglial properties147.”
From Microglia in neurodegeneration (2018) · cites this paper as [147]
The intestinal microbiota can regulate microglial maturation and function in the enteric and central nervous systems.
“Studies using germ-free mice, antibiotic treatment, and selective microbial colonization suggest that the intestinal microbiota can regulate microglial maturation and function in the enteric and central nervous systems [37, 54].”
From Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain (2022) · cites this paper as [37]
Germ-free mice develop microglia with an immature phenotype, blunted inflammatory response, and defective immune response to infection.
“Germ-free mice develop microglia with an immature phenotype, blunted response to inflammatory stimuli and defective immune response to infection (Erny et al., 2015).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Erny et al., 2015
Germ-free mice show microglia dysfunction that can be rescued by SCFA treatment.
“Germ-free mice exhibited microglia dysfunction that could be rescued by treatment with SCFAs.”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Erny et al., 2015
Ffar2−/− mice have a microglia defect similar to that of germ-free mice.
“Ffar2−/− mice had a similar defect, although no FFAR2 expression could be detected on microglia, leaving the connection between SCFAs and microglia unresolved (Erny et al., 2015).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Erny et al., 2015
SCFAs have functional importance for microglia, a macrophage-like cell type in the central nervous system.
“Beyond intestinal macrophages, SCFAs have also been reported to be functionally important for microglia, a macrophage-like cell type of the central nervous system.”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Erny et al., 2015
FFAR2 expression was not detected on microglia.
“although no FFAR2 expression could be detected on microglia”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Erny et al., 2015
A gut-brain axis exists involving neural and metabolic communication that could affect microglia.
“A gut-brain axis exists involving both neural and metabolic communication that could affect microglia199.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [199]
The host microbiome controls maturation and function of microglia.
“Finally, the microbiome plays a central role in health and disease, and the host microbiome controls maturation and function of microglia199.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [199]
Germ-free animals or mice treated with broad-spectrum antibiotics develop dysfunctional microglia, an effect ameliorated by short-chain fatty acids.
“Animals raised in a germ-free environment or mice treated with broad-spectrum antibiotics develop dysfunctional microglia, an effect that can be ameliorated with short-chain fatty acids.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [199]
Proper functioning of brain microglia needs the gut microbiome.
“Erny and colleagues [257] demonstrated that proper functioning of the brain microglia needs the gut microbiome.”
From The Role of Microbiota-Gut-Brain Axis in Neuropsychiatric and Neurological Disorders (2021) · cites this paper as [257]
The microbiome is required for proper development and function of adult brain microglia.
“Interestingly, Erny and colleagues demonstrate that the microbiome is required for proper development and function of adult brain microglia (71).”
From Emerging Roles for the Gut Microbiome in Autism Spectrum Disorder (2017) · cites this paper as [71]
Microbiota contributes to microglia homeostasis, potentially mediated by signaling through SCFAs.
“The microbiota contributes to microglia homeostasis, potentially mediated by signaling through SCFAs.240”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [240]
Germ-free mice display marked defects in microglia structure and function and hence feature impaired CNS innate immune responses.
“GF mice display marked defects in microglia structure and function and hence feature impaired CNS innate immune responses.240,241”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [240]
The microglial transcriptomic profile can be shaped by intrinsic factors such as age and sex, pathogenic and tissue-specific cues, and external cues such as microbiota signals.
“The transcriptomic profile can be shaped by intrinsic factors, such as age and sex, pathogenic and tissue-specific cues including protein aggregates, stress signals, nutrients, and external cues such as signals from the microbiota colonizing gastrointestinal and urogenital tracts [15].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
Microglial transcriptomes are tightly regulated by multiple key transcription factors such as Sall1, Spi1, Mafb, and Mef2c.
“Microglial transcriptomes are tightly regulated by multiple key transcription factors such as Sall1, Spi1, Mafb, and Mef2c [5, 15].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
Accumulating evidence indicates that PU.1 expression significantly alters microglia phenotypes via reshaping the gut microbiota landscape.
“Accumulating evidence indicates that PU.1 expression significantly alters the microglia phenotypes via reshaping the gut microbiota landscape.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
RNA-seq analysis of microglia from germ-free mice revealed that PU.1 and survival factor CSF1R were significantly upregulated.
“RNA-seq analysis of microglia from GF mice revealed that microglia transcription factor PU.1 and survival factor CSF1R were significantly upregulated in microglia from GF mice [1, 15].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
The immature phenotype of germ-free microglia could be corrected by microbiota recolonization.
“The immature phenotype of GF microglia could be corrected by microbiota recolonization [15].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
Gut symbiosis promotes microglial maintenance under homeostatic conditions.
“gut symbiosis promoted the maintenance of microglia under homeostasis conditions, while germ-free (GF) condition led to impaired microglia maturation, differentiation and function [15].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
Germ-free conditions lead to impaired microglial maturation, differentiation, and function.
“while germ-free (GF) condition led to impaired microglia maturation, differentiation and function [15].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
The gut microbiome has emerged as a key regulator of the immune system and microglial physiology.
“The gut microbiome has emerged as a key regulator of the immune system and microglial physiology.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
Microglia are dysregulated in mice with dysbiosis, either due to microbial imbalance or maladaptation.
“Microglia are dysregulated in mice with dysbiosis, either due to microbial imbalance or maladaptation [15]”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [15]
iMGLs grown without neurons differentially express early microglial genes, including FFAR2.
“iMGLs not cultured with neurons differentially expressed early microglia genes including FFAR2”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Erny et al., 2015
Microbes influence CNS processes via modulation of the nervous system, endocrine system, and immune system, together with their ability to synthesize neurotransmitters and produce metabolites.
“Microbes influence CNS processes via modulation of the nervous system (52), endocrine system (51, 126), and immune system (120), together with their ability to synthesize neurotransmitters (127–129) and produce metabolites (127, 130–132) ( Figure 1 ).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [120]
The GM appears to influence microglial development and maturation.
“The GM appears to influence microglial development and maturation (120, 121), and animal models have demonstrated downstream effects on various aspects of neurocognitive function (19, 45, 60, 114, 115).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [120]
SCFAs can modify neuroinflammation by affecting the morphology and function of glial cells.
“SCFAs can modify neuroinflammation by affecting the morphology and function of glial cells (120, 286, 289, 290).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [120]
Antibiotic-treated and germ-free mice have pro-inflammatory systemic and CNS immune responses.
“Antibiotic-treated and germ-free mice have pro-inflammatory systemic and CNS immune system responses (120, 267).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [120]
SCFAs may improve neuronal homeostasis and function by influencing neurotrophic factors such as nerve growth factor, glial cell line-derived neurotrophic factor, and BDNF.
“SCFAs may also improve neuronal homeostasis and function by influencing neurotrophic factors such as nerve growth factor, glial cell line-derived neurotrophic factor, and BDNF (119–122).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [120]
In germ-free mice, SCFA administration rescues deficits in microglial immaturity and morphology.
“By administering SCFAs to germ-free mice, Erny et al. were able to rescue deficits in microglial immaturity and morphology (120).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [120]
Impairments in microglia function were reversed by administration of SCFAs.
“Interestingly, impairments in microglia function were reversed by administration of SCFAs [38].”
From Role of diet and its effects on the gut microbiome in the pathophysiology of mental disorders (2022) · cites this paper as [38]
Germ-free mice had a decreased number of mature microglia in various brain areas compared to mice with a normal microbiome.
“In a rodent study, germ-free mice had a decreased number of mature microglia in various brain areas when compared to mice with a normal microbiome [38].”
From Role of diet and its effects on the gut microbiome in the pathophysiology of mental disorders (2022) · cites this paper as [38]
In the central nervous system, SCFAs regulate maturity and function of microglia.
“In the central nervous system, SCFAs have additional roles, such as regulating maturity and function of microglia (macrophages in the brain that are part of the brain’s immune response) [56].”
From Effect of fecal microbiota transplant on symptoms of psychiatric disorders: a systematic review (2020) · cites this paper as [56]
Innate immunity is regulated by the gut microbiota, as evidenced by reduced numbers and compromised functions of antigen-presenting cells and microglia in germ-free animals.
“Innate immunity is also regulated by the gut microbiota as evidenced by reduced numbers and compromised functions of antigen-presenting cells and microglia in germ-free animals60,69.”
From The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease (2018) · cites this paper as [60]
A lack of gut microbiota leads to deficient development of the GALT and abnormal systemic and central immunity.
“A lack of gut microbiota leads to deficient development of the GALT58 and abnormal systemic59 and central immunity60.”
From The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease (2018) · cites this paper as [60]
Treatment with microbial-produced short-chain fatty acids can rescue microglial function impaired in germ-free animals.
“A study demonstrated that treatment with microbial-produced short-chain fatty acids (SCFAs) could rescue microglial function impaired in GF animals [167].”
From Autism, Gastrointestinal Symptoms and Modulation of Gut Microbiota by Nutritional Interventions (2019) · cites this paper as [167]
GF mice display deficits in microglia maturation and function, while recolonization or administration of key gut microbiota metabolites such as SCFAs restore microglial function.
“Recent studies have shown that GF mice display deficits in microglia maturation and function, while recolonization or administration of key gut microbiota metabolites such as SCFAs restore microglial function”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Erny et al., 2015
FFAR2 transgenic mice have severely malformed microglia even though microglia do not express FFAR2, indicating that FFAR2 plays an indirect role in microglia function and homeostasis.
“In addition, FFAR2 transgenic mice have severely malformed microglia even though microglia do not express FFAR2, indicating that FFAR2 plays an indirect role in microglia function and homeostasis (Erny et al., 2015).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Erny et al., 2015
The absence of a complex host microbiota, when using GF animals or antibiotic-treated mice, increased microglial populations, caused defects in microglia maturation, activation state and differentiation, altered microglia morphology, and compromised immune response to bacterial or viral infection.
“In contrast, the absence of a complex host microbiota (when using GF animals or antibiotic-treated mice) increased microglial populations, caused defects in microglia maturation, activation state and differentiation, altered microglia morphology (with longer processes and increased branching, terminal points and clubbing at synaptic boutons), and compromised immune response to bacterial or viral”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Erny et al., 2015
Host microbiota control the maturation and function of microglia.
“This is supported by observations in mice, where host microbiota control the maturation and function of microglia 33 .”
From Transcriptomic analysis of purified human cortical microglia reveals age-associated changes (2017) · cites this paper as [33]
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- Authors
- Erny, D., Hrabě de Angelis, A. L., Jaitin, D., Wieghofer, P., Staszewski, O., David, E., Keren-Shaul, H., Mahlakoiv, T., Jakobshagen, K., Buch, T., Schwierzeck, V., Utermöhlen, O., Chun, E., Garrett, W. S., McCoy, K. D., Diefenbach, A., Staeheli, P., Stecher, B., Amit, I., & Prinz, M.
- Affiliations
- University of Freiburg (DE)
- Weizmann Institute of Science (IL)
- University of Cologne (DE)
- Technical University of Munich (DE)
- Johannes Gutenberg University Mainz (DE)
- Harvard University (US)
- University of Bern (CH)
- German Center for Infection Research (DE)
- Corresponding author
- Prinz, Marco
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2015-06-01
- Volume
- 18
- Issue
- 7
- Pages
- 965-977
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC5528863
- OpenAlex
- W1515023627
- Cited by
- 3,569
- References
- 61
- Citations by year
- 2026: 403 · 2025: 393 · 2024: 413 · 2023: 380 · 2022: 472 · 2021: 407 · 2020: 345 · 2019: 250 · 2018: 195 · 2017: 156 · 2016: 118 · 2015: 32 · 2014: 1
- FWCI
- 89.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- PubMed Central (acceptedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- OPUS (Augsburg University) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Deutsche Forschungsgemeinschaft (SFB 992, FOR1336)
- Bundesministerium für Bildung und Forschung
- National Cancer Institute (R01CA154426)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- host microbiota, microglia, microglial maturation, microglial homeostasis, germ-free mice, short-chain fatty acids, FFAR2, innate immune response, gut-brain axis, bacterial fermentation products, central nervous system
- MeSH terms
- Animals, Central Nervous System, Fatty Acids, Volatile, Female, Homeostasis, Immunity, Innate, Male, Mice, Inbred C57BL, Microglia, Receptors, G-Protein-Coupled, Mice, Microbiota
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