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.
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.
Department of Chemistry, Biotechnology and Food Science, The Norwegian University of Life Sciences, Ås, Norway. charlotte.kleiveland@umb.no
Charlotte R
CR
Kleiveland
Lene T Olsen
LT
Hult
Signe
S
Spetalen
Magne
M
Kaldhusdal
Trine Eker
TE
Christofferesen
Oskar
O
Bengtsson
Odd Helge
OH
Romarheim
Morten
M
Jacobsen
Tor
T
Lea
D000818:Animals; D056449:Bacillales / Q000502:physiology; D003093:Colitis, Ulcerative / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control; D003106:Colon / Q000382:microbiology* / Q000502:physiology; D016264:Dextran Sulfate / Q000633:toxicity*; D004032:Diet / Q000379:methods*; D004195:Disease Models, Animal; D007413:Intestinal Mucosa / Q000382:microbiology* / Q000502:physiology; D020619:Methylococcus capsulatus / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D055262:Mucin-2 / Q000378:metabolism; D043367:Ralstonia / Q000502:physiology
C524626:Muc2 protein, mouse; D055262:Mucin-2; D016264:Dextran Sulfate