Host-Pathogen Interaction in Colorectal Carcinogenesis

Dear Colleagues,

For many years it was generally accepted that multiple external environmental risk factors (such as alcohol, diet, life style, soil arsenic and nickel exposure), or hereditary traits, were involved in the development of colorectal cancer (CRC). More recently, mounting literature strongly suggests that alterations of a particular internal risk factor (i.e., dysbiosis in the luminal colonic microenvironment) might be crucial for generating the mucosal changes required for the evolution of sporadic and hereditary CRC.

This notion has been lately substantiated experimentally: gavage of fecal samples from patients with CRC to germ-free and conventional mice promoted intestinal carcinogenesis. Hence, the imbalance of the gut microbiota seems to play a substantial role in the evolution of CRC, not only in humans but also in laboratory animals. However, dysbiosis per se does not fulfil all requirements for that development; the bacterial species implicated in triggering colorectal carcinogenesis have to trespass the mucosal barrier, to reach the host. So far, the mechanisms whereby the gut microbiota reaches the host remains unclear. In inflammatory bowel disease (IBD), the breakdown of the integrity of barrier of macrophages in the lamina propria permits both toxic alien and commensal gut bacteria to trespass that barrier, resulting in host invasion. This leads to alteration of the natural host immunity (that critically controls intestinal carcinogensis) and the development of IBD-associated CRC. A similar defective mucosal barrier might also apply for patients with dysbiosis and hereditary or sporadic CRC.

For this Special Issue of Pathogens, we invite you to submit research articles, review articles, short notes as well as communications related to this part. We look forward to your contribution.

Prof. Carlos A Rubio
Guest Editor

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• Colorectal cancer
• CRC
• Gut microbiota
• Inflammatory bowel disease