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Review
. 2018 Aug 15:9:1830.
doi: 10.3389/fimmu.2018.01830. eCollection 2018.

Aspects of Gut Microbiota and Immune System Interactions in Infectious Diseases, Immunopathology, and Cancer

Affiliations
Review

Aspects of Gut Microbiota and Immune System Interactions in Infectious Diseases, Immunopathology, and Cancer

Veronica Lazar et al. Front Immunol. .

Abstract

The microbiota consists of a dynamic multispecies community of bacteria, fungi, archaea, and protozoans, bringing to the host organism a dowry of cells and genes more numerous than its own. Among the different non-sterile cavities, the human gut harbors the most complex microbiota, with a strong impact on host homeostasis and immunostasis, being thus essential for maintaining the health condition. In this review, we outline the roles of gut microbiota in immunity, starting with the background information supporting the further presentation of the implications of gut microbiota dysbiosis in host susceptibility to infections, hypersensitivity reactions, autoimmunity, chronic inflammation, and cancer. The role of diet and antibiotics in the occurrence of dysbiosis and its pathological consequences, as well as the potential of probiotics to restore eubiosis is also discussed.

Keywords: antibiotics; autoimmunity; cancer; chronic inflammation; diet; gut microbiota; opportunistic infections; probiotics.

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Figures

Figure 1
Figure 1
The host-microbiome interplay in colorectal cancer. Some bacterial species including Fusobacterium spp., Enterococcus spp., Escherichia coli, and Bacteroides spp. are most commonly associated with colorectal cancer. Changes in microbiota composition (dysbiosis) impair the gut barrier function of epithelial tight junctions and the mucus layer. Consequently, this increases the exposure of the epithelium to bacteria and their metabolites which may have carcinogenic potential. Bacterial translocation also leads to increased inflammation associated with the production of procarcinogens or toxic chemicals such as reactive oxygen species (ROS), bacterial genotoxins (colibactin), and hydrogen sulfide (H2S). Altogether, these changes trigger oxidative stress which leads to DNA damage. A series of pathways independent of the inflammatory response, but related to bacterial enzymes which could generate carcinogenic compounds, are cited in the literature by which the gastrointestinal microbiome may be involved in the genesis and evolution of neoplastic processes.

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