Oligomannan Prebiotic Attenuates Immunological, Clinical and Behavioral Symptoms in Mouse Model of Inflammatory Bowel Disease

Szilamér Ferenczi, Krisztián Szegi, Zsuzsanna Winkler, Teréz Barna, Krisztina J. Kovács

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Inflammatory bowel disease shows increasing prevalence, however its pathomechanism and treatment is not fully resolved. Prebiotics are non-digestible carbohydrates which might provide an alternative to treat inflammatory conditions in the gut due to their positive effects either on the microbiome or through their direct effect on macrophages and mucosa. To test the protective effects of an oligomannan prebiotic, yeast cell wall mannooligosaccharide (MOS) was administered in dextran-sulphate-sodium (DSS)-induced mouse model of acute colitis. MOS reduced DSS-induced clinical- (weight loss, diarrhea) and histological scores (mucosal damage) as well as sickness-related anxiety. DSS treatment resulted in changes in colon microbiome with selective increase of Coliform bacteria. MOS administration attenuated colitis-related increase of Coliforms, normalized colonic muc2 expression and attenuated local expression of proinflammatory cytokines IL-1a, IL1b, IL6, KC, G-CSF and MCP1 as well as toll-like receptor TLR4 and NLRP3 inflammasome. Some of the protective effects of MOS were likely be mediated directly through local macrophages because MOS dose-dependently inhibited IL-1b and G-CSF induction following in vitro DSS challenge and IL1a, IL1b, G-SCF-, and IL6 increases after LPS treatment in mouse macrophage cell line RAW264.7. These results highlight oligomannan prebiotics as therapeutic functional food for testing in clinical trials.

Original languageEnglish
Article number34132
JournalScientific reports
Volume6
DOIs
Publication statusPublished - Sep 23 2016

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Oligomannan Prebiotic Attenuates Immunological, Clinical and Behavioral Symptoms in Mouse Model of Inflammatory Bowel Disease'. Together they form a unique fingerprint.

  • Cite this