VvpE mediates the intestinal colonization of Vibrio vulnificus by the disruption of tight junctions
International Journal of Medical Microbiology, ISSN: 1438-4221, Vol: 306, Issue: 1, Page: 10-19
2016
- 22Citations
- 27Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations22
- Citation Indexes22
- 22
- CrossRef18
- Captures27
- Readers27
- 27
Article Description
The disruption of gastrointestinal tight junctions and their colonization evoked by enteric pathogens are hallmarks of the pathogenesis. Vibrio ( V. ) vulnificus, VvpE, is an elastase which is responsible for host surface adherence and vascular permeability; however, the functional roles of VvpE in the pathogenesis of V. vulnificus (WT) are poorly understood. In the present study, we have investigated the role of VvpE in regulation of intestinal tight junctions and the colonization of WT. We found that mutation of the vvpE gene from V. vulnificus ( vvpE mutant) prevents intestinal tight/adherens junction dysregulation due to a WT infection and maintains the physiological level of the epithelial paracellular permeability. Interestingly, the vvpE mutant exhibited defective intestinal colonization abilities, whereas WT colonization was significantly elevated in the ileum in a time-dependent manner. Finally, the vvpE mutant negated the enterotoxicity, the breakdown of red blood cells, and pro-inflammatory responses, all of which are induced by the WT infection. In addition, the results of a LC–MS/MS analysis showed that VvpE contributes to WT pathogenesis in multiple ways by interacting with intestinal proteins, including β-globin, Annexin A2, Annexin A4, F-actin, and intelectin-1b. These results demonstrate that VvpE plays important role in promoting the tight junction disruption and intestinal colonization of V. vulnificus and that it also has the ability to interact with the intestinal proteins responsible for microbial pathogenesis.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1438422115300163; http://dx.doi.org/10.1016/j.ijmm.2015.10.006; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84953334994&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/26552364; https://linkinghub.elsevier.com/retrieve/pii/S1438422115300163; https://dx.doi.org/10.1016/j.ijmm.2015.10.006
Elsevier BV
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