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Review
.2019 Jan 3;26(1):1.
doi: 10.1186/s12929-018-0495-4.

Pathobiont release from dysbiotic gut microbiota biofilms in intestinal inflammatory diseases: a role for iron?

Affiliations
Review

Pathobiont release from dysbiotic gut microbiota biofilms in intestinal inflammatory diseases: a role for iron?

Andre Gerald Buret et al. J Biomed Sci..

Abstract

Gut microbiota interacting with an intact mucosal surface are key to the maintenance of homeostasis and health. This review discusses the current state of knowledge of the biofilm mode of growth of these microbiota communities, and how in turn their disruptions may cause disease. Beyond alterations of relative microbial abundance and diversity, the aim of the review is to focus on the disruptions of the microbiota biofilm structure and function, the dispersion of commensal bacteria, and the mechanisms whereby these dispersed commensals may become pathobionts. Recent findings have linked iron acquisition to the expression of virulence factors in gut commensals that have become pathobionts. Causal studies are emerging, and mechanisms common to enteropathogen-induced disruptions, as well as those reported for Inflammatory Bowel Disease and colo-rectal cancer are used as examples to illustrate the great translational potential of such research. These new observations shed new light on our attempts to develop new therapies that are able to protect and restore gut microbiota homeostasis in the many disease conditions that have been linked to microbiota dysbiosis.

Keywords: Campylobacter; Colo-rectal cancer; Crohn’s disease; Dysbiosis; Enteropathogen; Giardia; Inflammatory bowel disease; Iron; Metabolome; Microbiome; Microbiota biofilm; Mucus; Pathobionts; Post-infectious IBS.

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Conflict of interest statement

Ethics approval and consent to participate

This sreview article did not require experimentation.

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All authors have read and approved this article for publication.

Competing interests

The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1
Gut Microbiota live as biofilms: a) Confocal laser micrograph of microbiota grown form a healthy human donor colonic biopsy ex vivo on the Calgary Biofilm Device ™, and illustrating their biofilm mode of growth (A3, merge image). The microbiota visibly contain a thick exopolysaccharide coating typical of bacterial biofilms (A2, wheat germ agglutinin stain) covering live bacteria (A1). Bars = 20 μm. B) Human microbiota biofilms grown on the Calgary Biofilm Device ™ and observed under scanning electron microscopy. The slimy exopolysaccharide coating of the biofilm hides underlying bacterial morphology in healthy conditions (B1), and this exopolysaccharide can be lost upon exposure to an enteropathogen likeGiardia sp. (B2). C) Gut microbiota in the colon of a healthy rat, illustrating the biofilm sheet formed by the commensals (red), separated from the epithelial surface (blue) by the intestinal mucus barrier (not stained). Bar = 50 μm.
Fig. 2
Fig. 2
Dysbiotic microbiota (red) in rats with experimental colitis induced by DNBS (B and C) compared to control non-inflamed tissue (a). Fragments of the dysbiotic microbiota biofilm (b,c, in red) directly adhere to the epithelial surface (blue), and releases invasive pahobionts seen in the process of translocation (arrows). Bars = 50 μm. (Modified from reference 20)
Fig. 3
Fig. 3
Enteropathogen-induced abnormalities of the colonic microbiota biofilm phenotype (green) is associated with disruption of the mucus barrier (red) in mice infected withGiardia sp. for 7 days (b), compared to control tissue (a). This provides researchers with a powerful model to investigate the mechanisms and consequences of gut microbiota biofilm disruptions, and subsequent invasion of pathobionts. Bars = 200 μm). (Modified from reference 36)
Fig. 4
Fig. 4
Confical laser micrographs of human microbiota (red) grown on the Calgary Biofilm Device and then incubated with human intestinal epithelial cells (green). Biofilm bacteria dispersed from microbiota of donors with Crohn’s Disease readily translocate (arrows) across the monolayers (b) whereas bacteria from microbiota of healthy donors do not (a). Bars = 20 μm)
Fig. 5
Fig. 5
Schematic diagram illustrating the complex pathogen-commensal-mucus-tissue interactions discussed in this review. Microbiota biofilm disruption and pathobiont dispersion cause diseases resulting from microbiota dysbiosis. The data collected to support this model focus on enteropathogen-induced microbiota dysbiosis, and the microbiota disruptions reported in Inflammatory Bowel Disease and colo-rectal cancer. 1) Biofilm fragments of the microbiota cross the mucus barrier and adhere to the epithelial surface. 2) Planktonic bacteria dispersed from the microbiota biofilm may act as virulent pathobionts; adherent and motile pathobionts release pathogenic compounds (ie hemolysin,hlyE gene), and express genes involved in epithelial adhesion (egfimA,sfmF, fliD). 3) Transformation of commensal microbiota bacteria into pathobionts is enabled at least in part through microbial uptake of excess iron from the intestinal environment. 4–5) Pathobionts translocate through the epithelium paracellularly [4] and transcellularly [5]. 6) Pathobionts activate host immunity to cause post-infectious and inflammatory disorders, or to exacerbate and/or cause inflammation in Inflammatory Bowel Disease, or to induce colorectal cancer
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References

    1. Sender R, Fuchs S, Milo R. Revised estimates for the number of human and bacteria cells in the body. PLoS Boil. 2016;14(18):e1002533. doi: 10.1371/journal.pbio.1002533. - DOI - PMC - PubMed
    1. Gordon JI. Honor thy gut symbionts redux. Science. 2012;336:1251–1253. doi: 10.1126/science.1224686. - DOI - PubMed
    1. Sprockett D, Fukami T, Relman DA. Role of priority effects in the early-life assembly of the gut microbiota. Nature Rev Gastroenterol Hepatol. 2018;15:197–205. doi: 10.1038/nrgastro.2017.173. - DOI - PMC - PubMed
    1. Backhed F, Fraser CM, Ringel Y, Sanders ME, Sartor RB, Sherman PM, Versalovic J, Yoiung V, Finlay BB. Defining a healthy human gut microbiome: current concepts, future directions, and clinical applications. Cell Host Micr. 2012;12:611–622. doi: 10.1016/j.chom.2012.10.012. - DOI - PubMed
    1. Sartor RB, Wu GD. Roles for intestinal bacteria, viruses, and fungi in pathogenesis of inflammatory bowel diseases and therapeutic approaches. Gastroenterology. 2017;152:327–329. doi: 10.1053/j.gastro.2016.10.012. - DOI - PMC - PubMed

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