Journal
ALIMENTARY PHARMACOLOGY & THERAPEUTICS
Volume 43, Issue -, Pages 27-36Publisher
WILEY
DOI: 10.1111/apt.13436
Keywords
-
Funding
- Salix
Ask authors/readers for more resources
BackgroundGut microbiota dysbiosis contributes to the pathogenesis of inflammatory bowel diseases (IBD). Although the microbiota's role in IBD pathogenesis, specifically Crohn's disease (CD), provides a rationale for antibiotic treatment, antibiotic use in CD remains controversial. Rifaximin, traditionally identified as a nonsystemic bactericidal antibiotic, may be therapeutically beneficial for inducing CD remission. AimTo examine the role of rifaximin in the management of IBD and its potential mechanisms of action. MethodsA literature search using the following strategy: (inflammatory bowel disease' OR Crohn's' OR ulcerative'), rifaximin' AND (barrier' OR translocation' OR adhesion' OR internalization' OR pregnane X'), AND pregnane X' AND (Crohn's' OR ulcerative colitis' OR inflammatory bowel disease'). ResultsIn vitro data suggest rifaximin mediates changes in epithelial cell physiology and reduces bacterial attachment and internalisation. In experimental colitis models, rifaximin antagonised the effects of tumour necrosis factor- on intestinal epithelial cells by activating pregnane X receptor, which inhibits nuclear factor-B-mediated proinflammatory mediators and induces detoxification genes (e.g. multidrug resistance 1 and cytochrome P450 3A4). Rifaximin also inhibits bacterial translocation into the mesenteric lymph nodes. ConclusionAccumulating evidence suggests that mechanisms of action of rifaximin in IBD may not be limited to direct bactericidal activity; therefore, rifaximin could potentially be redefined as a gut environment modulator.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available