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Bifidobacteria confer protection against NSAID‐enteropathy independently of acetate production
Author(s) -
Syer Stephanie D.,
Martin Rebeca,
McKnight G. Webb,
Langella Philippe,
Wallace John L.
Publication year - 2013
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.27.1_supplement.1093.4
Subject(s) - bifidobacterium longum , chemistry , naproxen , strain (injury) , bifidobacterium breve , enteropathy , food science , microbiology and biotechnology , bifidobacterium , biology , fermentation , medicine , pathology , alternative medicine , disease , lactobacillus
Rats were orally treated with vehicle or Bifidobacterium longum subsp. Adolescentis (BA), a low acetate producer, or B. longum subsp. longum (BL), a high acetate producer (both at 10 9 CFU), for 9 days. In addition, two isogenic strains were also tested: a second BL strain (BN) and its derivative (BNKO) in which a gene deletion results in low acetate production. Naproxen (20 mg/kg) was co‐administered on the final 4 days, then small intestinal damage was blindly scored. Treatment with BA decreased naproxen‐induced intestinal damage by 82%; p<0.05, while BL exerted no effect. BN reduced damage by 75% (p<0.05), and a similar beneficial effect was observed with the low acetate‐producing knockout bacterium, BNKO (62% reduction; p<0.05). Small intestinal injury by NSAIDs is a serious clinical problem, with no available treatments. Acetate production by these Bifidobacterium strains does not appear to be important for prevention of NSAID‐enteropathy, given that a high acetate producing Bifidobacteria (BL) exhibited no protective effect, while a low acetate‐producing mutant (BNKO) was as effective in reducing damage as another high acetate‐producing bacterium (BN).