Abstract Title:

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

Abstract Source:

Carcinogenesis. 2014 Dec 30. Epub 2014 Dec 30. PMID: 25550315

Abstract Author(s):

Michael Doulberis, Katerina Angelopoulou, Eleni Kaldrymidou, Anastasia Tsingotjidou, Zaphiris Abas, Susan E Erdman, Theofilos Poutahidis

Article Affiliation:

Michael Doulberis


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

Study Type : Bacterial

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