NSAID enteropathy and bacteria: a complicated relationship
Open accessAbstract
The clinical significance of small intestinal damage caused by nonsteroidal anti-inflammatory drugs (NSAIDs) remains under-appreciated. It occurs with greater frequency than the damage caused by these drugs in the upper gastrointestinal tract, but is much more difficult to diagnose and treat. Although the pathogenesis of NSAID enteropathy remains incompletely understood, it is clear that bacteria, bile, and the enterohepatic circulation of NSAIDs are all important factors. However, they are also interrelated with one another. Bacterial enzymes can affect the cytotoxicity of bile and are essential for enterohepatic circulation of NSAIDs. Gram-negative bacteria appear to be particularly important in the pathogenesis of NSAID enteropathy, possibly through release of endotoxin. Inhibitors of gastric acid secretion significantly aggravate NSAID enteropathy, and this effect is due to significant changes in the intestinal microbiome. Treatment with antibiotics can, in some circumstances, reduce the severity of NSAID enteropathy, but published results are inconsistent. Specific antibiotic-induced changes in the microbiota have not been causally linked to prevention of intestinal damage. Treatment with probiotics, particularly Bifidobacterium, Lactobacillus, and Faecalibacteriaum prausnitzii, has shown promising effects in animal models. Our studies suggest that these beneficial effects are due to colonization by the bacteria, rather than to products released by the bacteria.
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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.
“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].”
From Proton pump inhibitors and dysbiosis: current knowledge and aspects to be clarified (2019) · cites this paper as [100]
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References 47 · Cited by 80
- Authors
- Syer, S. D., Blackler, R. W., Martin, R., de Palma, G., Rossi, L., Verdu, E., Bercik, P., Surette, M. G., Aucouturier, A., Langella, P., & Wallace, J. L.
- Affiliations
- McMaster University (CA)
- Microbiologie de l’alimentation au service de la santé (FR)
- University of Calgary (CA)
- Corresponding author
- Wallace, John L.
- Venue
- Journal of Gastroenterology
- Published
- 2015-01-10
- Volume
- 50
- Issue
- 4
- Pages
- 387-393
- ISSN
- 0944-1174 (ISSN-L)
- 1435-5922
- OpenAlex
- W2027039192
- Cited by
- 80
- References
- 47
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 13 · 2020: 6 · 2019: 9 · 2018: 12 · 2017: 11 · 2016: 5 · 2015: 3
- FWCI
- 1.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- HAL (submittedVersion, cc-by)
- Funders
- McKnight Foundation
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- NSAID-induced enteropathy, nonsteroidal anti-inflammatory drugs, small bowel injury, intestinal bacteria, bile, enterohepatic circulation, Gram-negative bacteria, endotoxin, gastric acid secretion inhibitors, gut microbiota, antibiotic therapy, probiotics, Faecalibacterium prausnitzii, Lactobacillus, Bifidobacterium, bacterial colonization
- MeSH terms
- Anti-Inflammatory Agents, Non-Steroidal, Anti-Bacterial Agents, Humans, Intestinal Diseases, Intestine, Small, Ulcer, Probiotics, Host-Pathogen Interactions, Microbiota
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