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Review
. 2015 May 21;11(5):e1004787.
doi: 10.1371/journal.ppat.1004787. eCollection 2015 May.

Intestinal Colonization Dynamics of Vibrio cholerae

Affiliations
Review

Intestinal Colonization Dynamics of Vibrio cholerae

Salvador Almagro-Moreno et al. PLoS Pathog. .

Abstract

To cause the diarrheal disease cholera, Vibrio cholerae must effectively colonize the small intestine. In order to do so, the bacterium needs to successfully travel through the stomach and withstand the presence of agents such as bile and antimicrobial peptides in the intestinal lumen and mucus. The bacterial cells penetrate the viscous mucus layer covering the epithelium and attach and proliferate on its surface. In this review, we discuss recent developments and known aspects of the early stages of V. cholerae intestinal colonization and highlight areas that remain to be fully understood. We propose mechanisms and postulate a model that covers some of the steps that are required in order for the bacterium to efficiently colonize the human host. A deeper understanding of the colonization dynamics of V. cholerae and other intestinal pathogens will provide us with a variety of novel targets and strategies to avoid the diseases caused by these organisms.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Model for intestinal colonization dynamics of V. cholerae.
V. cholerae may be ingested as free-living cells (i), as forming microcolonies (ii), or as part of a biofilm (iii) (A). Cells in the lumen will first come in contact with the mucus layer (B). The bacterium must reach the intestinal epithelium by penetrating through the viscous mucus layer covering it (C). Once the bacterium reaches the intestinal epithelium, we hypothesize that noncommitted (reversible) attachment occurs, mediated by adhesins such as GbpA or Mam7 (D). Subsequently, specific attachment adhesins might be produced that would allow V. cholerae to bind in a committed fashion (E), the cells multiply (F), and, once a certain concentration of cells has been reached, the toxin coregulated pilus is produced, allowing for microcolony formation and toxin production (G).

References

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