Therapeutic effects and the possible mechanism of fecal transplantation on rats with Clostridium diffi-cile-associated pseudomembranous colitis / 中华微生物学和免疫学杂志

ABSTRACT

Objective To investigate the therapeutic effects and the possible mechanism of fecal transplantation on rats with Clostridium difficile-associated pseudomembranous colitis. Methods A total of 40 Sprague-Dawley rats were divided into four groups including the healthy control group, model group, fecal transplant treatment group and vancomycin treatment group. Rats in three experimental groups were subcuta-neously injected with clindamycin phosphate (10 mg), followed by treatment with toxin producing Clostridi-um difficile (ACTT43255) enema 24 hours later. The rats in fecal transplant treatment group and vancomy-cin treatment group were respectively treated with fecal suspension and vancomycin one day after modeling. The rats were fasted for one day after the last administration and then executed. The levels of potassium ion ( K) , sodium ion ( Na) , albumin ( ALB) , white blood cells ( WBC) , C-reaction protein ( CRP) , interleu-kin-1β ( IL-1β) , interleukin-10 ( IL-10 ) , interleukin-12 ( IL-12 ) and interleukin-17 ( IL-17 ) as well as the percentage of neutrophils ( N%) in serum samples were detected. The colon tissue samples were collect-ed for pathology examination. Results The rat model of pseudomembranous colitis was successfully estab-lished by subcutaneous injection of clindamycin in combination with toxin-producing Clostridium difficile (ACTT43255) enema. The signs of intestinal inflammation including serious weight loss, remarkably short-ened colon length and significantly increased colon wet weight index were observed in rats from the model group (P<0. 05). Compared with the rats from model group, the rats received fecal transplant showed sig-nificantly increased levels of K, ALB, IL-10 and IL-10/IL-12 in serum and decreased levels of WBC, N%, CRP, IL-1β and IL-17 (P<0. 05). Conclusion Fecal transplantation was proved to be an effective ap-proach for the treatment of pseudomembranous colitis. The therapeutic mechanism might due to its impacts on serum inflammatory factors.