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Review
. 2014 Jan 28;20(4):908-22.
doi: 10.3748/wjg.v20.i4.908.

Inflammation and colorectal cancer, when microbiota-host mutualism breaks

Marco Candela  1 , Silvia Turroni  1 , Elena Biagi  1 , Franck Carbonero  1 , Simone Rampelli  1 , Carla Fiorentini  1 , Patrizia Brigidi  1
Affiliations
Review

Inflammation and colorectal cancer, when microbiota-host mutualism breaks

Marco Candela et al. World J Gastroenterol. .

Abstract

Structural changes in the gut microbial community have been shown to accompany the progressive development of colorectal cancer. In this review we discuss recent hypotheses on the mechanisms involved in the bacteria-mediated carcinogenesis, as well as the triggering factors favoring the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. The possible role of inflammation, bacterial toxins and toxic microbiota metabolites in colorectal cancer onset is specifically discussed. On the other hand, the strategic role of inflammation as the keystone factor in driving microbiota to become carcinogenic is suggested. As a common outcome of different environmental and endogenous triggers, such as diet, aging, pathogen infection or genetic predisposition, inflammation can compromise the microbiota-host mutualism, forcing the increase of pathobionts at the expense of health-promoting groups, and allowing the microbiota to acquire an overall pro-inflammatory configuration. Consolidating inflammation in the gut, and favoring the bloom of toxigenic bacterial drivers, these changes in the gut microbial ecosystem have been suggested as pivotal in promoting carcinogenesis. In this context, it will become of primary importance to implement dietary or probiotics-based interventions aimed at preserving the microbiota-host mutualism along aging, counteracting deviations that favor a pro-carcinogenic microbiota asset.

Keywords: Co-abundance groups; Colorectal cancer; Gut microbiome; Inflammation.

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Figures

Figure 1
Figure 1
Network plot showing correlation relationships among clusters of bacterial genera for the Wu et al[80] dataset. Each node represents a taxon color-coded for co-abundance group and each line highlights a significant correlation between two bacterial genera. Circle size is proportional to genus abundance. Solid lines indicate positive correlation, whereas dot lines indicate negative correlation. Thickness of the lines is proportional to correlation strength.
Figure 2
Figure 2
Colorectal cancer arises from the interplay between endogenous and exogenous factors, such as inflammation, diet, intestinal microbiome structure, and transcription and activity of bacterial genotoxins.
Figure 3
Figure 3
Environmental triggers, such as diet, aging and pathogen infections, can force microbiota changings that, in a genetically susceptible host, can drive to chronic inflammation in the gut. Inflammation shifts the gut microbiota towards a pro-inflammatory configuration, supporting colorectal cancer (CRC) drivers as pathobionts at the expense of health-promoting CRC-protective microbiota components. As a consequence, a pro-inflammatory loop is established in the gut, directly supporting CRC onset and favoring colonization by toxigenic bacterial drivers directly involved in CRC promotion.
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