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The noncommensal bacterium Methylococcus capsulatus (Bath) ameliorates dextran sulfate (Sodium Salt)-Induced Ulcerative Colitis by influencing mechanisms essential for maintenance of the colonic barrier function.

Abstract
Dietary inclusion of a bacterial meal has recently been shown to efficiently abolish soybean meal-induced enteritis in Atlantic salmon. The objective of this study was to investigate whether inclusion of this bacterial meal in the diet could abrogate disease development in a murine model of epithelial injury and colitis and thus possibly have therapeutic potential in human inflammatory bowel disease. C57BL/6N mice were fed ad libitum a control diet or an experimental diet containing 254 g/kg of body weight BioProtein, a bacterial meal consisting of Methylococcus capsulatus (Bath), together with the heterogenic bacteria Ralstonia sp., Brevibacillus agri, and Aneurinibacillus sp. At day 8, colitis was induced by 3.5% dextran sulfate sodium (DSS) ad libitum in the drinking water for 6 days. Symptoms of DSS treatment were less profound after prophylactic treatment with the diet containing the BioProtein. Colitis-associated parameters such as reduced body weight, colon shortening, and epithelial damage also showed significant improvement. Levels of acute-phase reactants, proteins whose plasma concentrations increase in response to inflammation, and neutrophil infiltration were reduced. On the other, increased epithelial cell proliferation and enhanced mucin 2 (Muc2) transcription indicated improved integrity of the colonic epithelial layer. BioProtein mainly consists of Methylococcus capsulatus (Bath) (88%). The results that we obtained when using a bacterial meal consisting of M. capsulatus (Bath) were similar to those obtained when using BioProtein in the DSS model. Our results show that a bacterial meal of the noncommensal bacterium M. capsulatus (Bath) has the potential to attenuate DSS-induced colitis in mice by enhancing colonic barrier function, as judged by increased epithelial proliferation and increased Muc2 transcription.
AuthorsCharlotte R Kleiveland, Lene T Olsen Hult, Signe Spetalen, Magne Kaldhusdal, Trine Eker Christofferesen, Oskar Bengtsson, Odd Helge Romarheim, Morten Jacobsen, Tor Lea
JournalApplied and environmental microbiology (Appl Environ Microbiol) Vol. 79 Issue 1 Pg. 48-56 (Jan 2013) ISSN: 1098-5336 [Electronic] United States
PMID23064342 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Muc2 protein, mouse
  • Mucin-2
  • Dextran Sulfate
Topics
  • Animals
  • Bacillales (physiology)
  • Colitis, Ulcerative (chemically induced, pathology, prevention & control)
  • Colon (microbiology, physiology)
  • Dextran Sulfate (toxicity)
  • Diet (methods)
  • Disease Models, Animal
  • Intestinal Mucosa (microbiology, physiology)
  • Methylococcus capsulatus (physiology)
  • Mice
  • Mice, Inbred C57BL
  • Mucin-2 (metabolism)
  • Ralstonia (physiology)

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