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Gut Pathogens  2011 

Bacillus Coagulans GBI-30 (BC30) improves indices of Clostridium difficile-Induced colitis in mice

DOI: 10.1186/1757-4749-3-16

Keywords: Clostridium difficile, probiotics, colitis, mice

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Abstract:

All mice treated with BC30 survived on study day 13, while two mice treated with vehicle did not survive. On day 12, a significant difference (p = 0.0002) in the percentage of mice with normal stools (66.7%) was found in the BC30/C. difficile group, as compared to the vehicle/C. diffcile group (13.0%). On study day 16, 23.8% of mice treated with BC30 had normal stools, while this value was 0% with vehicle treatment (p value = 0.0187). On this day, the stool consistency score for the BC30/C. difficile group (1.1 ± 0.2) was significantly lower (p < 0.05) than for the vehicle/C. difficile cohort (1.9 ± 0.2). BC30 modestly attenuated the colonic pathology (crypt damage, edema, leukocyte influx) that was present following C. difficile infection. Colonic MIP-2 chemokine contents (pg/2 cm colon) were: 10.2 ± 0.5 (vehicle/no C. difficile), 24.6 ± 9.5 (vehicle/C. difficile) and 16.3 ± 4.3 (BC30/C. difficle).The probiotic BC30 improved some parameters of C. difficile-induced colitis in mice. BC30 prolonged the survival of C. diffiicle infected mice. Particularly, this probiotic improved the stool consistency of mice, in this infectious colitis model.Clostridium Difficile (C. difficile) infection can cause nosocomial-related diarrhea [1]. The spectrum of C. difficile-associated disease (CDAD) ranges from mild antibiotic associated diarrhea to severe (or even life threatening) pseudomembranous colitis [1]. CDAD is caused by the actions of two exotoxins (toxin A and toxin B), which are produced by pathogenic strains of C. difficile [2,3].Previous data suggests that toxin A can activate the nuclear factor-kappa B (NF-κB) signal transduction system in monocytes and colonic epithelial cells [4,5]. This activation of NF-κB leads to secretion of a key pro-inflammatory chemokine (IL-8) and subsequently to neutrophil influx into the colonic tissue [4,5]. Neutrophils play a key role in the pathogenesis of CDAD, both in humans and in mice [6].CDAD is often treated successfully with stand

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