Bacillus coagulans GBI-30, 6086 limits the recurrence of Clostridium difficile-Induced colitis following vancomycin withdrawal in mice

The mean stool consistency score in Vehicle/C.difficile/Vanco mice increased from 0.4 (day 10) to a range of 1.1 to 1.4 (days 14 to 17), indicating the recurrence of colitis. On days 13 through 17, the stool consistency scores for the vancomycin/BC30 mice were significantly lower (p< 0.05) than for the vancomycin/vehicle cohort of animals. On day 17, 88.9% of mice treated with BC30 had normal stools, while this value was 0% with vehicle treatment (p value = 0.0004). Colonic myeloperoxidase (Units/2 cm colon) was significantly (p < 0.05) reduced from 4.3 ± 0.7 (Vehicle/C.difficile/Vanco) to 2.6 ± 0.2 (BC30/C. Difficle/Vanco). The colonic histology score and Keratinocyte derived-chemokine level in the colon were also lower in BC30 treated mice.In BC30-treated mice, there was evidence of better stool consistency, as well as improved biochemical and histological indices of colitis, following initial treatment of animals with vancomycin.BC30 limited the recurrence of CD-induced colitis following vancomycin withdrawal in mice.Clostridium difficile (C. difficile) infection (CDI) is a very common cause of health-care associated diarrhea and colitis [1]. Moreover, CDI is associated with significant morbidity, as well as increased health care costs [2]. The spectrum of C. difficile associated disease (CDAD) ranges from mild antibiotic associated diarrhea to severe and life threatening pseudomembranous colitis [3]. CDAD is caused by the actions of two toxins (toxin A and toxin B), which are produced by pathogenic strains of C. difficile[4,5]. Toxin A results in the activation of three transcription factors (NF- kB, AP1 and CREB). NF-kB (nuclear factor-kappa B) is involved in chemokine production, and also plays a role in colonocyte apoptosis [6,7]. AP-1 (activator protein-1) plays a role in IL-8 production in response to stimulation of colonocytes with toxin A [8]. CREB (Cyclic-AMP Response Binding Protein) is critical for the production of prostaglandin E2 via inducible cyclo