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World J Gastroenterol. Jan 28, 2014; 20(4): 908-922
Published online Jan 28, 2014. doi: 10.3748/wjg.v20.i4.908
Inflammation and colorectal cancer, when microbiota-host mutualism breaks
Marco Candela, Silvia Turroni, Elena Biagi, Franck Carbonero, Simone Rampelli, Carla Fiorentini, Patrizia Brigidi
Marco Candela, Silvia Turroni, Elena Biagi, Simone Rampelli, Patrizia Brigidi, Department of Pharmacy and Biotechnology, University of Bologna, 40126 Bologna, Italy
Franck Carbonero, Department of Food Science, University of Arkansas, Fayetteville, AR 72704, United States
Carla Fiorentini, Department of Therapeutic Research and Medicines Evaluation, Istituto Superiore di Sanità, 00161 Rome, Italy
Author contributions: Candela M conceived and designed the article, and wrote the manuscript; Turroni S, Biagi E, Carbonero F, Fiorentini C reviewed literature, wrote the manuscript, revised and edited the draft; Rampelli S performed bioinformatics analysis; Brigidi P reviewed and edited the final version of the article; all Authors read and approved the final version of the manuscript.
Correspondence to: Marco Candela, PhD, Department of Pharmacy and Biotechnology, University of Bologna, Via Belmeloro 6, 40126 Bologna, Italy. marco.candela@unibo.it
Telephone: +39-51-2099727 Fax: +39-51-2099734
Received: September 27, 2013
Revised: November 26, 2013
Accepted: December 12, 2013
Published online: January 28, 2014
Processing time: 121 Days and 2.2 Hours
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: Colorectal cancer; Inflammation; Gut microbiome; Co-abundance groups

Core tip: By performing the co-abundance groups analysis of the publicly available datasets from microbiome surveys in colorectal cancer (CRC) patients, we have been successful in identifying pro-carcinogenic and protective groups of microorganisms, showing the potential to modulate the fate of CRC onset and progression. Possible mechanisms involved in microbiota-dependent carcinogenesis are reviewed, and the central role of inflammation as a trigger forcing the microbiota from a mutualistic configuration to a CRC-promoting asset is discussed. Finally, possible intervention strategies for modulating microbiome in order to preserve its mutualistic configuration along life span are suggested.