Cholera-toxin suppresses carcinogenesis in a mouse model of inflammation-driven sporadic colon cancer

摘要: Human studies and clues from animal models have provided important links between gastrointestinal (GI) tract bacteria colon cancer. Gut microbiota antigenic stimuli play an role in shaping the intestinal immune responses. Therefore, especially case of inflammation-associated cancer, gut antigens may affect tumorigenesis. The present study aimed to investigate effects oral administration a bacterial product with known immunomodulatory properties on inflammation-driven colorectal neoplasmatogenesis. For that, we used cholera-toxin well-established mouse model cancer which neoplasia is initiated by single dose genotoxic agent azoxymethane (AOM) subsequently promoted inflammation caused colitogenic substance dextran sodium sulfate (DSS). We found that single, low, non-pathogenic CT, given orally at beginning each DSS treatment cycle downregulated neutrophils upregulated regulatory T-cells IL-10 colonic mucosa. CT-induced disruption tumor-promoting character DSS-induced led reduction AOM-initiated polypoidogenesis. This result adds value emerging notion certain GI or their products system render microenvironment preneoplastic lesions less favorable for promoting evolution