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The human milk oligosaccharide, 2'‐fucosyllactose, quenches Campylobacter jejuni ‐induced inflammation in intestinal mucosa
Author(s) -
Yu ZhuoTeng,
Nanthakumar N Nanda,
Newburg David
Publication year - 2015
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.29.1_supplement.853.6
Subject(s) - campylobacter jejuni , immune system , campylobacter , microbiology and biotechnology , ex vivo , in vivo , inflammation , immunology , intestinal mucosa , pathogenesis , biology , ingestion , proinflammatory cytokine , medicine , bacteria , endocrinology , genetics
Background Campylobacter jejuni causes diarrhea worldwide; young children are most susceptible. C. jejuni binding to intestinal mucosa is inhibited ex vivo by α1,2‐fucosylated carbohydrate moieties, including human milk oligosaccharides (hMOS). 2'‐fucosyllactose (2'‐FL) is the simplest α1,2‐fucosylated hMOS, and is predominant in most human milks. Methods: The ability of 2'‐FL to inhibit C. jejuni infection and subsequent inflammation in vitro was tested in HEp‐2 and HT 29 human epithelial cells (HEC). A new murine model of Campylobacter infection was developed, validated, and used to test the ability of 2'‐FL to inhibit Campylobacter infection in vivo .Results: 2'‐FL inhibited C. jejuni infection of HEC, and suppressed release of mucosal proinflammatory signals IL‐8, IL‐1β and the neutrophil chemoattractant MIP‐2. In mice inoculated with C. jejuni, ingestion of 2'‐FL reduced Campylobacter colonization and weight loss, diminished histologic features of intestinal inflammation, and attenuated induction of inflammatory signaling molecules of the acute phase mucosal immune response. This acute model did not perturb IL‐17 (adaptive T‐cell response). Conclusions 2'‐FL inhibits pathogenesis of human C. jejuni and its sequelae in HEC and in a novel murine model. 2'‐FL may represent a new class of oral agents for prevention and treatment of specific enteric infectious diseases.