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Semin Immunol. 2017 Aug;32:43-53. doi: 10.1016/j.smim.2017.09.006. Epub 2017 Oct 2.

Microbiome, inflammation and colorectal cancer.

Author information

1
Department of Immunology, School of Medicine, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT, 06030, United States.
2
Department of Immunology, School of Medicine, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT, 06030, United States. Electronic address: kewang@uchc.edu.

Abstract

Chronic inflammation is linked to the development of multiple cancers, including those of the colon. Inflammation in the gut induces carcinogenic mutagenesis and promotes colorectal cancer initiation. Additionally, myeloid and lymphoid cells infiltrate established tumors and propagate so called "tumor-elicited inflammation", which in turn favors cancer development by supporting the survival and proliferation of cancer cells. In addition to the interaction between cancer cells and tumor infiltrating immune cells, the gut also hosts trillions of bacteria and other microbes, whose roles in colorectal inflammation and cancer have only been appreciated in the past decade or so. Commensal and pathobiotic bacteria promote colorectal cancer development by exploiting tumor surface barrier defects following cancer initiation, by invading normal colonic tissue and inducing local inflammation, and by generating genotoxicity against colonic epithelial cells to accelerate their oncogenic transformation. On the other hand, a balanced population of microbiota is important for the prevention of colorectal cancer due to their roles in providing certain bacterial metabolites and inhibiting intestinal inflammation. In this review we summarize our current knowledge regarding the link between microbiota, inflammation, and colorectal cancer, and aim to delineate the mechanisms by which gut microbiome and inflammatory cytokines regulate colorectal tumorigenesis.

KEYWORDS:

Bacteria; Colorectal cancer; Inflammation; Microbiota

PMID:
28982615
DOI:
10.1016/j.smim.2017.09.006
[Indexed for MEDLINE]

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