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5‐HT disturbs interaction between gut epithelium and commensal bacteria (653.10)
Author(s) -
Regmi Sushil,
Shadfar Sina,
Neupane Ganesh,
Lee Jintae,
Lee JinHyung,
Kim JungAe
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.653.10
Subject(s) - microbiology and biotechnology , gut flora , immune system , biology , intestinal epithelium , proinflammatory cytokine , interleukin 22 , microbiome , immunology , nadph oxidase , bacteria , inflammation , epithelium , cytokine , interleukin , reactive oxygen species , bioinformatics , genetics
The gut is considered as one of immune privilege sites, which is developed by complex interplay between gut microbiome and the intestinal epithelial barrier. The mechanisms regulating gut tolerance to the commensal bacteria also play an important role in the protection of intestine against epithelial injury. Human studies in patients with inflammatory bowel disease (IBD) have implicated aberrant communication between host and gut flora such as inappropriate immune responses against their own flora. In addition to the excessive production of proinflammatory cytokines, serotonin (5‐hydroxytryptamine, 5‐HT), an enteric neurotransmitter and paracrine hormone, is also increased in the gut of IBD patients, suggesting its role in the pathogenesis of IBD. In the present study, we examined the role of 5‐HT in aberrant communication between gut epithelial cells and commensal bacteria ( E coli ). 5‐HT enhanced adherence of commensal E coli to HT29 colonic epithelial cells without affecting the adherence of pathogenic E coli . At the same time, 5‐HT treatment synergistically increased mRNA expression of IL‐8, TLR‐2, and Nox2 in commensal E coli ‐treated‐HT29 cells. Either pretreatment with NADPH oxidase inhibitor (DPI) and antioxidant (vitamin C) or transfection with Nox2 siRNA significantly suppressed the 5‐HT‐induced adhesion of commensal E coli to HT‐29 cells. Taken together, 5‐HT disturbs the interaction between gut epithelium and commensal bacteria, which may alter gut tolerance to commensal bacteria. Grant Funding Source : Supported by Basic Science Research Program through the National Research Foundati