AI Article Synopsis

  • Colorectal cancer (CRC) is a leading cause of cancer deaths worldwide, with colonic inflammation and microbiota playing significant roles in its development.
  • Research shows that specific gut bacteria can either promote inflammation and cancer or help protect against them by modulating immune responses.
  • The interaction between gut microbiota and immune systems is complex, influencing inflammation and CRC through various signaling pathways, which could lead to new microbiota-based treatments for colitis and CRC.

Article Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer-related death in the world. Besides genetic causes, colonic inflammation is one of the major risk factors for CRC development, which is synergistically regulated by multiple components, including innate and adaptive immune cells, cytokine signaling, and microbiota. The complex interaction between CRC and the gut microbiome has emerged as an important area of current CRC research. Metagenomic profiling has identified a number of prominent CRC-associated bacteria that are enriched in CRC patients, linking the microbiota composition to colitis and cancer development. Some microbiota species have been reported to promote colitis and CRC development in preclinical models, while a few others are identified as immune modulators to induce potent protective immunity against colitis and CRC. Mechanistically, microbiota regulates the activation of different immune cell populations, inflammation, and CRC crosstalk between innate and adaptive immune signaling pathways, including nuclear factor kappa B (NF-κB), type I interferon, and inflammasome. In this review, we provide an overview of the potential interactions between gut microbiota and host immunity and how their crosstalk could synergistically regulate inflammation and CRC, thus highlighting the potential roles and mechanisms of gut microbiota in the development of microbiota-based therapies to prevent or alleviate colitis and CRC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9373904PMC
http://dx.doi.org/10.3389/fimmu.2022.963819DOI Listing

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