Proton pump inhibitors and dysbiosis: current knowledge and aspects to be clarified
Open accessAbstract
., dysbiosis). The gut microbiota is a complex ecosystem in which microbes coexist and interact with the human host. Indeed, the resident gut bacteria are needed for multiple vital functions, such as nutrient and drug metabolism, the production of energy, defense against pathogens, the modulation of the immune system and support of the integrity of the gut mucosal barrier. The bacteria are collected in communities that vary in density and composition within each segment of the gastrointestinal (GI) tract. Therefore, every change in the gut ecosystem has been connected to an increased susceptibility or exacerbation of various GI disorders. The aim of this review is to summarize the recently available data on PPI-related microbiota alterations in each segment of the GI tract and to analyze the possible involvement of PPIs in the pathogenesis of several specific GI diseases.
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Written from the paper’s full text.
TL;DR
This narrative review summarizes evidence that proton pump inhibitors, through long-term acid suppression, alter gut microbiota composition across the gastrointestinal tract and may contribute to dysbiosis-associated diseases. It concludes that PPIs should be used only when strictly necessary and that further prospective studies are needed to clarify health impacts.
Key findings
- PPIs reduce gastric acid and alter microbiota in each GI segment; a four-week esomeprazole study in healthy volunteers increased *Fusobacterium* and *Leptotrichia* in the periodontal pocket, decreased *Neisseria* and *Veillonella* in saliva, and increased *Streptococcus* in fecal samples.
- In the stomach, *Streptococcaceae* were the most abundant family during PPI therapy; hypochlorhydria reduced microbial diversity and increased nitrate/nitrite reductase bacterial functions. One study reported up to 2.4 times greater gastric cancer risk in long-term PPI users even after *H. pylori* eradication, though other meta-analyses did not confirm this risk.
- Chronic PPIs strongly impact the small intestine and can cause small intestinal bacterial overgrowth, defined as more than 10^5 bacteria per ml of upper gut aspirate; PPI-induced dysbiosis may increase risk of hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis. In rats, PPIs reduced jejunal *Actinobacteria* and *Bifidobacteria* spp. and exacerbated NSAID-induced enteropathy.
- In the colon, PPIs decrease commensal bacteria and microbial diversity and increase oral bacteria in stool; they are associated with increased *Clostridium difficile* infection and other enteric infections and may predispose to IBS. Post-infectious IBS occurs in 10%-30% of patients after infectious gastroenteritis, while many studies found no direct correlation between PPI use and colorectal cancer.
Methods
- Design: narrative review.
- Data or sample: no primary data; synthesizes published literature on PPI-related microbiota alterations in each GI tract segment and specific GI diseases.
- Main analysis: narrative synthesis; no systematic search strategy, databases, inclusion/exclusion criteria, or quantitative meta-analysis are reported.
Limitations
- The paper states that further prospective studies are necessary to define how PPI-induced microbial changes impact human health, that confirmation in humans is needed for the role of dysbiosis in NSAID enteropathy, and that the validity of probiotic prevention remains to be seen.
- The paper notes ongoing uncertainty: the role of PPIs in gastric cancer development is under debate, IBD microbial data are not fully elucidated, and many studies have not found a direct correlation between PPI use and colorectal cancer.
- Evident from the text: as a narrative review, it lacks a systematic search, formal quality appraisal, and meta-analysis, so findings are synthesized without formal bias assessment.
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Integrity signals
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Cites
Statistics
Claims the paper makes
0 of 99 cited sources checked · 0 supported · 0 flagged
- Premisecitation
Changes in microbial equilibrium (dysbiosis) can promote and influence the course of many intestinal and extra-intestinal diseases.
“Changes in this microbial equilibrium that is, dysbiosis can promote and influence the course of many intestinal and extra-intestinal diseases[14-16].”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationcitation
Campylobacter concisus could have a role in EAC, promoting the metaplastic processes in the early stages of cancer through an increase in IL-18 expression and downregulation of TGF-beta1, NF-κB and STAT3 signaling involved in the EAC cascade.
“This bacterium could have a role in EAC, promoting the metaplastic processes in the early stages of cancer through an increase in the interleukin (IL)-18 expression and downregulation of transforming growth factor beta 1, nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 signaling involved in the EAC cascade[42-44].”
Quote in the paperNot a substantial claim0 of 3 sources checked - Premisecitation
Long-term use of PPIs exposes patients to an increased risk of developing extra-intestinal disorders.
“The use of PPIs is generally well tolerated, although their long-term use exposes patients to an increased risk of developing extra-intestinal disorders[6-8]”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
PPI-driven gastric hypochlorhydria can cause significant changes in gut microbiota composition.
“likely due to PPI-driven gastric hypo-chlorhydria, which can cause also significant changes in gut microbiota composition[9-11]”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Long-term use of PPIs is associated with an increased risk of EAC in the absence of other risk factors.
“A recent epidemiological study revealed that, in the absence of other risk factors, the long-term use of PPIs is associated with an increased risk of EAC[48].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [48] source
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- Premisecitation
In both ERD and BE, a significant enrichment of Campylobacter concisus has been reported.
“In both these conditions, a significant enrichment of Campylobacter concisus has been reported[42,43].”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
Other meta-analyses do not confirm an increased risk of GC in long-term PPI users.
“and other meta-analyses not confirming such a risk[65,66]”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [65] source
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- cites [66] Eslami L, Nasseri-Moghaddam S. Meta-analyses: Does long-term PPI use increase the risk of gastric premalignant lesions? Arch Iran Med 2013; 16: 449-458
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- Premisecitation
Several studies have shown that bacterial migration from the antrum to gastric body and fundus occurs more frequently during long-term PPIs use.
“Several studies have shown that the bacterial migration from the antrum to gastric body and fundus occurs more frequently during long-term PPIs use[71].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [71] source
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- Interpretationcitation
Through the induction of different metabolic pathways, such bacteria could have a role in gastric cancer (GC) progression.
“Through the induction of different metabolic pathways, such bacteria could have a role in gastric cancer (GC) progression[61].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [61] source
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- Premisecitation
Some of the microbial changes caused by PPIs are the same as the alterations already present in patients with cirrhosis and especially in patients with decompensated cirrhosis, including the relative increase of potentially pathogenic bacteria such as Staphylococcaeae, Enterobacteriaceae and Enterococcaceae.
“It is noteworthy that some of the microbial changes caused by PPIs are the same as the alterations already present in patients with cirrhosis and especially in patients with decompensated cirrhosis including the relative increase of potentially pathogenic bacteria such as Staphylococcaeae, Enterobacteriaceae and Enterococcaceae[93].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [93] source
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- Premisecitation
During H. pylori infection, the gastric microbiota is predominantly constituted of Proteobacteria, followed by Firmicutes, Bacteroidetes and Actinobacteria.
“During the infection, the gastric microbiota is predominantly constituted of Proteobacteria, followed by Firmicutes, Bacteroidetes and Actinobacteria[54].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [54] source
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- Premisecitation
In rats, a PPI-driven significant reduction of Actinobacteria and Bifidobacteria spp. in the jejunum was shown to exacerbate NSAID-induced enteropathy.
“In rats, a PPI-driven significant reduction of Actinobacteria and Bifidobacteria spp. in the jejunum was shown to exacerbate NSAID-induced enteropathy[98].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [98] source
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- Premisecitation
High gastric pH values can give rise to a different bacterial balance characterized by a significant increase in oral bacteria, such as Peptostreptococcus stomatis, Streptococcus anginosus, Parvimonas micra, Slackia exigua and Dialister pneumosintes.
“Moreover, high gastric pH values can give rise to a different bacterial balance characterized by a significant increase in oral bacteria, such as Pepto-streptococcus stomatis, Streptococcus anginosus, Parvimonas micra, Slackia exigua and Dialister pneumosintes.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [61] source
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- Premisecitation
Streptococcaceae are the most abundant family observed during PPI therapy, followed by Prevotellaceae, Campylobacteraceae and Leptotrichiaceae.
“Streptococcaceae are the most abundant family observed during PPI therapy, followed by Prevotellaceae, Campylobacteraceae and Leptotrichiaceae[58].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [58] source
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- Premisecitation
In jejunal samples of SIBO patients, an overgrowth of microaerophilic microorganisms such as Streptococcus, Staphylococcus, Escherichia, and Klebsiella and anaerobic bacteria such as Bacteroides, Lactobacillus, Veillonella and Clostridium was found.
“In jejunal samples of SIBO patients, an overgrowth of microaerophilic microorganisms such as Streptococcus, Staphylococcus, Escherichia, and Klebsiella and anaerobic bacteria such as Bacteroides, Lactobacillus, Veillonella and Clostridium was found[85].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [85] source
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- Premisecitation
Long-term PPI use significantly decreases the risk of progression to high-grade dysplasia and EAC in patients with non-dysplastic BE.
“because their long-term use significantly decreases the risk of the progression to high-grade dysplasia and EAC[50-52]”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
PPIs have also been reported to exacerbate the mucosal damage caused by NSAIDs in the distal portion of the small bowel to the ligament of Treitz.
“PPIs have also been reported to exacerbate the mucosal damage caused by non-steroidal anti-inflammatory drugs (NSAIDs) in the distal portion of the small bowel to the ligament of Treitz[95,96]”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
PPI-induced dysbiosis may represent a risk factor for hepatic encephalopathy (HE) and spontaneous bacterial peritonitis (SBP) in cirrhotic patients.
“PPI-induced dysbiosis may represent a risk factor for hepatic encephalopathy (HE) and spontaneous bacterial peritonitis (SBP) in cirrhotic patients[88-90].”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
Many studies over the years have not found a direct correlation between PPI use in clinical practice and an increased risk of CRC.
“Nevertheless, it is fundamental to highlight that many studies over the years have not found a direct correlation between PPI use in clinical practice and an increased risk of CRC[154-156].”
Quote in the paperNot a substantial claim0 of 3 sources checked - Interpretationcitation
The expansion of Proteobacteria could facilitate a mucosal immune response in genetically predisposed individuals, leading to the development and continuation of chronic intestinal inflammation.
“Moreover, the expansion of Proteobacteria could facilitate a mucosal immune response in genetically predisposed individuals, leading to the development and continuation of chronic intestinal inflammation[133,142,143].”
Quote in the paperNot a substantial claim0 of 3 sources checked - Interpretationreasoning
In the context of dysbiosis, PPIs may lead to short-term flare ups in the course of IBDs.
“In the context of dysbiosis, PPIs may lead to short-term flare ups in the course of IBDs.”
Quote in the paperNot a substantial claim - Premisecitation
Chronic hypergastrinemia, typically present during PPI use, can promote the growth of malignant colonic epithelial cells, facilitating the deleterious sequencing adenoma-carcinoma.
“Last, chronic hypergastrinemia, typically present during PPI use, can promote the growth of malignant colonic epithelial cells, facilitating the deleterious sequencing adenoma-carcinoma[151-153].”
Quote in the paperNot a substantial claim0 of 3 sources checked - Interpretationcitation
It is likely that PPI use predisposes patients to the development of IBS.
“It is likely that PPI use predisposes patients to the development of IBS[116].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [116] source
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- Premisecitation
IBD patients are particularly susceptible to the development of bacterial superinfections, especially those caused by Clostridium difficile, Campylobacter, Salmonella, Shigella and Entamoeba histolytica, which represent harmful stimuli that can induce a relapse of the disease in a microenvironment that is already altered.
“This is likely because IBD patients are particularly susceptible to the development of bacterial superinfections, especially those caused by Clostridium difficile, Campylobacter, Salmonella, Shigella and Entamoeba histolytica, which represent harmful stimuli that can induce a relapse of the disease in a microenvironment that is already altered[140,141].”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
The consequence of F. nucleatum invasion is the promotion of NF-κB signaling and the expression of several cytokines, such as IL-6, IL-8, IL-10, IL-18 and TNF-α.
“The consequence of this invasion is the promotion of NF-κB signaling and the expression of several cytokines, such as IL-6, IL-8, IL-10, IL-18 and TNF-α.”
Quote in the paperSubstantial claim0 of 2 sources checked
- May combine two claims. 27
- Classified as probably not a substantial claim. 5
May combine two claims.
PremisecitationIn healthy volunteers, a four-week esomeprazole administration caused an increase of Fusobacterium and Leptotrichia in the periodontal pocket, associated with a decrease of Neisseria and Veillonella in saliva and a parallel increase of Streptococcus in fecal samples.
“One study showed that, in healthy volunteers, a four-week esomeprazole administration of PPI caused an increase of Fusobacterium and Leptotrichia in the periodontal pocket, associated with a decrease of Neisseria and Veillonella in saliva and a parallel increase of Streptococcus in fecal samples”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [34] source
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Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationPPIs are the first-choice treatment for acid-related disorders such as bleeding, peptic ulcers, gastroesophageal reflux, erosive esophagitis (ERD) and certain dyspepsia subtypes.
“PPIs are the first-choice treatment for acid-related disorders such as bleeding, peptic ulcers, gastroesophageal reflux, erosive esophagitis (ERD) and certain dyspepsia subtypes[2-5].”
Quote in the paperNot a substantial claim0 of 4 sources checkedMay combine two claims.
InterpretationcitationThe switch in favor of Gram-negative bacteria in the esophagus could cause an LPS-mediated activation of innate immunity, inducing a dangerous cycle of dysbiosis-inflammation-dysbiosis and mucosal damage.
“It is likely that this switch in favor of Gram-negative bacteria could cause an LPS-mediated activation of innate immunity, inducing a dangerous cycle of dysbiosis-inflammation-dysbiosis and mucosal damage[38].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [38] source
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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationProton pump inhibitors (PPIs) are acid-suppressive agents and are among the most widely used and over-used drugs in the world.
“Proton pump inhibitors (PPIs) are acid-suppressive agents and are among the most widely used and over-used drugs in the world[1].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [1] source
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PremisecitationThe gut microbiota has a key role in metabolic, nutritional, physiological, defensive and immunological processes in the human body.
“The gut microbiota has a key role in metabolic, nutritional, physiological, defensive and immunological processes in the human body, and its composition is closely connected to individuals’ health and the diseases they experience[12,13].”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
InterpretationcitationThe oral cavity could represent a potential source of microbiota information related to oral and non-oral disorders; it could also be an important indicator of dysbiosis in other areas of the GI tract.
“Based on these data, the oral cavity could represent a potential source of microbiota information related to oral and non-oral disorders; it could also be an important indicator of dysbiosis in other areas of the GI tract.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationPPI treatment can alter esophageal microbiota, causing an increase in the abundance of Firmicutes and a decrease in the abundance of Bacteroidetes and Proteobacteria.
“PPI treatment can alter esophageal microbiota, causing an increase in the abundance of Firmicutes and a decrease in the abundance of Bacteroidetes and Proteobacteria[47].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [47] source
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PremisecitationTwo types of microbiota have been identified in the esophagus: Type I, present in healthy subjects, is characterized by a predominance of Gram-positive taxa (especially Streptococcus), whereas type II, associated with ERD and Barrett esophagus (BE), is constituted by a predominance of Gram-negative taxa, including Veillonella, Prevotella, Haemophilus, Neisseria, Rothia, Granulicatella, Campylobact
“two types of microbiota have been identified in the esophagus: Type I, present in healthy subjects, is characterized by a predominance of Gram-positive taxa (especially Streptococcus), whereas type II, associated with ERD and Barrett esophagus (BE), is constituted by a predominance of Gram-negative taxa”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationThe distal esophagus is mostly colonized by Firmicutes, followed by Bacteroidetes, Actinobacteria, Proteobacteria and Fusobacteria, with the most represented genera being Streptococcus, followed by Prevotella and Veillonella.
“The distal tract is mostly colonized by Firmicutes, followed by Bacteroidetes, Actinobacteria, Proteobacteria and Fusobacteria, with the most represented genera being Streptococcus, followed by Prevotella and Veillonella[35].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [35] source
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InterpretationcitationPPIs may cause both oral and gut microbiota alterations.
“this suggests that PPIs may cause both oral and gut microbiota alterations[34]”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [34] source
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PremisecitationBoth ERD and BE are considered precursor conditions to esophageal adenocarcinoma (EAC).
“Both ERD and BE are considered precursor conditions to esophageal adenocarcinoma (EAC)[41].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [41] source
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PremisecitationSome studies and meta-analyses report an increased risk of developing GC in long-term PPI users up to 2.4 times greater, even after H. pylori eradication.
“with some studies and meta-analyses reporting an increased risk of developing GC in long-term PPI users[62,63] up to 2.4 times greater, even after Helicobacter pylori (H. pylori) eradication, according to a recent study[64]”
Quote in the paperNot a substantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationThe primary abundance of Streptococcaceae was also demonstrated in dyspeptic patients during PPI treatment, suggesting that this ecological switch in favor of Streptococcaceae could be an independent indicator of gastric dysbiosis due to these drugs.
“The primary abundance of Streptococcaceae was also demonstrated in dyspeptic patients during PPI treatment, suggesting that this ecological switch in favor of Streptococcaceae could be an independent indicator of gastric dysbiosis due to these drugs[59].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [59] source
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PremisecitationGerm-free mice are less susceptible to intestinal lesions induced by NSAIDs and NSAID-induced enteropathy is transferable via microbiota.
“Moreover, germ-free mice are less susceptible to intestinal lesions induced by NSAIDs and it has been documented that NSAID-induced enteropathy is transferable via microbiota[98,101,102].”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationH. pylori infection can lead to antrum-predominant gastritis, in which the oxyntic mucosa is not inflamed but a gastrin-driven increase in acid output occurs, along with the possible development of duodenal ulcer.
“H. pylori infection can lead to antrum-predominant gastritis, in which the oxyntic mucosa is not inflamed but a gastrin-driven increase in acid output occurs, along with the possible development of duodenal ulcer[67,68].”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationHypochlorhydria promotes a reduction in microbial diversity and the growth of microbes that have genotoxic potential, with an increase in the nitrate/nitrite reductase bacterial functions involved in cancer development.
“It is important to keep in mind that hypochlorhydria promotes a reduction in microbial diversity and the growth of microbes that have genotoxic potential, with an increase in the nitrate/nitrite reductase bacterial functions involved in cancer development[60].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [60] source
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PremisecitationWhen H. pylori infection spreads to the oxyntic mucosa, it causes pangastritis, which is associated with hypochloridria, and is responsible for the development of chronic atrophic gastritis, intestinal metaplasia and, finally, dysplasia and GC.
“In addition, when the infection does spread to the oxyntic mucosa, it causes pangastritis, which is associated with hypochloridria, and is responsible for the development of chronic atrophic gastritis, intestinal metaplasia and, finally, dysplasia and GC[69,70].”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationChronic treatment with PPIs strongly impacts small intestine microbiota and, in particular, causes small intestinal bacterial overgrowth (SIBO), likely due to the loss of the gastric acid defensive barrier.
“Chronic treatment with PPIs strongly impacts small intestine microbiota and, in particular, causes small intestinal bacterial overgrowth (SIBO), likely due to the loss of the gastric acid defensive barrier[81-83].”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationPPIs augmented the expression of bacteria with beta-glucuronidases activity, and this microbial imbalance could promote the spread of NSAIDs into enterohepatic circulation, increasing bile cytotoxicity and subsequently causing ulcerative lesions.
“Moreover, PPIs augmented the expression of bacteria with beta-glucuronidases activity, and this microbial imbalance could promote the spread of NSAIDs into enterohepatic circulation, increasing bile cytotoxicity and subsequently causing ulcerative lesions[99,100].”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationThe gastric microbiota is composed mainly of Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria, with the most abundant genera being Streptococcus, followed by Veillonella, Prevotella, Fusobacterium and Rothia.
“The gastric microbiota is composed mainly of Firmicutes, Bacteroidetes, Proteo-bacteria and Actinobacteria, with the most abundant genera being Streptococcus, followed by Veillonella, Prevotella, Fusobacterium and Rothia[54].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [54] source
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May combine two claims.
PremisecitationPPIs have unfavorable effects on gastric functions and host defensive mechanisms, causing delayed gastric emptying, decreased gastric mucus viscosity, increased bacterial load and increased bacterial translocation.
“PPIs have unfavorable effects on gastric functions and host defensive mechanisms, causing delayed gastric emptying, decreased gastric mucus viscosity, increased bacterial load and increased bacterial translocation[55-57].”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
InterpretationreasoningGastric hypochlorhydria caused by PPIs favors the survival and migration of oral bacteria in lower areas of the GI tract, with a possible establishment of a pro-inflammatory microenvironment.
“Moreover, the gastric hypochlorhydria caused by PPIs favors the survival and migration of oral bacteria in lower areas of the GI tract, with a possible establishment of a pro-inflammatory microenvironment.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationPPIs by reducing gastric acid secretion can produce profound changes in the colonic microbiota, mainly characterized by a decrease in the abundance of commensal bacteria, which is associated with a reduction in microbial diversity and an increase of oral bacteria in the stool.
“PPIs by reducing gastric acid secretion can produce profound changes in the colonic microbiota, mainly characterized by a decrease in the abundance of commensal bacteria, which is associated with a reduction in microbial diversity and an increase of oral bacteria in the stool[108,109].”
Quote in the paperSubstantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S1 (asserted).
PremisecitationIn CDI, a reduction in alpha diversity and a decrease in the abundance of bacteria of the Ruminococcoceae associated with an increase in the Enterobacteriaceae, Enterococcoceae and Lactobacillaceae families observed during long-term PPI treatment could facilitate the onset of infection.
“Even if not fully clarified, it has been hypothesized that, in CDI, a reduction in alpha diversity and a decrease in the abundance of bacteria of the Ruminococcoceae associated with an increase in the Enterobacteriaceae, Enterococcoceae and Lactobacillaceae families observed during long-term PPI treatment could facilitate the onset of infection[109].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [109] source
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InterpretationcitationLong-term PPI use facilitates the induction of enteric infection, and, through secondary changes in microbiota composition, these drugs may influence gut-brain axis functions, prompting IBS onset.
“As previously stated, the long-term PPI use facilitates the induction of enteric infection, and, through secondary changes in microbiota composition, these drugs may influence gut–brain axis functions, prompting IBS onset[117,118].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [117] source
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- cites [118] Carabotti M, Scirocco A, Maselli MA, Severi C. The gut-brain axis: Interactions between enteric microbiota, central and enteric nervous systems. Ann Gastroenterol 2015; 28: 203-209
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PremisecitationF. nucleatum has two adhesion proteins, FapA and FadA, the latter of which mediates the invasion of the bacterium into the intestinal epithelium.
“This microorganism has two adhesion proteins, FapA and FadA, the latter of which mediates the invasion of the bacterium into the intestinal epithelium.”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationPPIs can influence the onset of enteric infections, resulting in an increased risk of Clostridium difficile infection (CDI), as well as Salmonella, Campylobacter and diarrheagenic Escherichia coli.
“PPIs can influence the onset of enteric infections, resulting in an increased risk of Clostridium difficile infection (CDI), as well as Salmonella, Campylobacter and diarrheagenic Escherichia coli (E. coli)[110-113].”
Quote in the paperSubstantial claim0 of 4 sources checkedMay combine two claims.
PremisecitationThe net result of these changes is the creation of a pro-inflammatory milieu for tumor growth, favored by the FapA-mediated suppression of T cells' cytotoxic activity.
“The net result of these changes is the creation of a pro-inflammatory milieu for tumor growth, favored by the FapA-mediated suppression of T cells’ cytotoxic activity[147,150].”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationF. nucleatum is a commensal anaerobic bacterium of the oral cavity associated with periodontal disorders, and it has been found in large quantities in CRC.
“F. nucleatum is a commensal anaerobic bacterium of the oral cavity associated with periodontal disorders, and it has been found in large quantities in CRC[147].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [147] source
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InterpretationreasoningThe evidence indicates that PPIs, likely through their acid-antisecretory effects, are able to modify the host microbiota in each segment of the GI tract and can contribute to dysbiosis development; this dysbiosis can, in turn, facilitate the onset of certain GI disorders.
“The evidence indicates that PPIs which are widely used in gastroenterology clinical practice likely through their acid-antisecretory effects, are able to modify the host microbiota in each segment of the GI tract and can contribute to dysbiosis development; this dysbiosis can, in turn, facilitate the onset of certain GI disorders.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationThe IBS dysbiosis mostly consists of a reduction in alpha diversity and an imbalance between microbial groups, represented by a scarce amount Bifidobacteria and Lactobacilli members and an increase in potentially pathogenic Enterobacteriaceae, such as E. coli.
“The IBS dysbiosis mostly consists of a reduction in alpha diversity and an imbalance between microbial groups, represented by a scarce amount Bifidobacteria and Lactobacilli members and an increase in potentially pathogenic Enterobacteriaceae, such as E. coli[127,128]”
Quote in the paperSubstantial claim0 of 2 sources checked
The paper relies on this without support.
Gastric dysbiosis occurs as a result of H. pylori-related gastritis.
“Gastric dysbiosis occurs as a result of H. pylori-related gastritis.”
The paper relies on this without support.
H. pylori pro-inflammatory activity affects the luminal microenvironment and modifies the gastric microbiota.
“H. pylori pro-inflammatory activity affects the luminal microenvironment and modifies the gastric microbiota.”
The paper relies on this without support.
Depending on the site of H. pylori colonization, the dysbiosis can be associated with either an increase or decrease in acid secretion, which further influences gastric microbiota composition.
“It is noteworthy that, depending on the site of H. pylori colonization, the dysbiosis can be associated with either an increase or decrease in acid secretion, which further influences gastric microbiota composition.”
The paper relies on this without support.
This dysbiosis has also been shown to be related to the occurrence of HE and SBP, implying a poor prognosis and disease progression.
“This dysbiosis has also been shown to be related to the occurrence of HE and SBP, implying a poor prognosis and disease progression.”
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?
Outcomes for proton pump inhibitors vary, with some studies showing no association.
“Outcomes vary, with some studies showing no association.”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [446]
Proton pump inhibitors have been shown to cause dysbiosis and are associated with cognitive decline.
“Another group of drugs that has been shown to cause dysbiosis and is associated with cognitive decline is the proton pump inhibitors (PPI) (446, 447).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [446]
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Revised Estimates for the Number of Human and Bacteria Cells in the Body
Sender, R., Fuchs, S., & Milo, R. (2016) · PLOS Biology · doi:10.1371/journal.pbio.1002533 · Cited by 5,425 · see citing works
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- Authors
- Bruno, G., Zaccari, P., Rocco, G., Scalese, G., Panetta, C., Porowska, B., Pontone, S., & Severi, C.
- Affiliations
- University of Otago (NZ)
- Corresponding author
- Pontone, Stefano
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2019-06-14
- Volume
- 25
- Issue
- 22
- Pages
- 2706-2719
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC6580352
- OpenAlex
- W2950297440
- Semantic Scholar
- 8c9a916b6bbfed0cf31d78d22613750fe17a7b02
- Cited by
- 258
- References
- 163
- Citations by year
- 2026: 19 · 2025: 31 · 2024: 46 · 2023: 62 · 2022: 31 · 2021: 37 · 2020: 27 · 2019: 4
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Gastroenterology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by-nc)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Surgery › Helicobacter pylori-related gastroenterology studies
- Keywords
- proton pump inhibitors, gut dysbiosis, gut microbiota, gastrointestinal diseases, gut mucosal barrier, immunomodulation, pathogenesis
- MeSH terms
- Gastrointestinal Microbiome, Achlorhydria, Bacteria, Gastric Acid, Gastric Mucosa, Humans, Intestinal Mucosa, Proton Pump Inhibitors, Dysbiosis
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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