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Review
. 2019 Jun;12(6):846-851.
doi: 10.1016/j.tranon.2019.03.003. Epub 2019 Apr 12.

Fusobacterium nucleatum Contributes to the Carcinogenesis of Colorectal Cancer by Inducing Inflammation and Suppressing Host Immunity

Jiao Wu  1 , Qing Li  1 , Xiangsheng Fu  2
Affiliations
Review

Fusobacterium nucleatum Contributes to the Carcinogenesis of Colorectal Cancer by Inducing Inflammation and Suppressing Host Immunity

Jiao Wu et al. Transl Oncol. 2019 Jun.

Abstract

The presence of Fusobacterium nucleatum (F. nucleatum) in the gut is associated with the development of colorectal cancer (CRC). F. nucleatum promotes tumor development by inducing inflammation and host immune response in the CRC microenvironment. Adhesion to the intestinal epithelium by the cell surface proteins FadA, Fap2 and RadD expressed by F. nucleatum can cause the host to produce inflammatory factors and recruit inflammatory cells, creating an environment which favors tumor growth. Furthermore, F. nucleatum can induce immune suppression of gut mucosa by suppressing the function of immune cells such as macrophages, T cells and natural killer cells, contributing the progression of CRC.

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Figures

Figure 1
Figure 1
Infiltrating immune cell populations in human F. nucleatum related colorectal cancer. High abundance of F. nucleatum within colon cancer tissue (A) and matched metastatic lymph nodes (B) detected by immunofluorescence. High density of immune cells (CD3+, CD68+, CD83+, and NE cells) within the environment of F. nucleatum-positive colon cancers (immunofluorescence). NE, neutrophils.
Figure 2
Figure 2
F. nucleatum induces a pro-inflammatory microenvironment and suppression of host immunity that favor tumor growth within the gut mucosa. F. nucleatum binds to colon epithelium through FadA, Fap2 and RadD, and invades the mucosa. This invasion by F. nucleatum increases the infiltration of inflammatory cells and the release of cytokines which stimulate cell proliferation. Moreover, invasive F. nucleatum interacts with the immune cells in the colon mucosa, resulting in the decrease of T cell density, increased M2 macrophage polarization, inhibition of NK cell activity, and the increase of dendritic cells and tumor-associated neutrophils that diminish anti-tumor immunity. The inhibition of mucosa immunity favors tumor progression.
See this image and copyright information in PMC

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