Aeromonas salmonicida Ati2 is an effector protein of the type three secretion system

Microbiology ◽  
2013 ◽  
Vol 159 (Pt_9) ◽  
pp. 1937-1945 ◽  
Author(s):  
Stéphanie Dallaire-Dufresne ◽  
Xavier Barbeau ◽  
Darren Sarty ◽  
Katherine H. Tanaka ◽  
Alix M. Denoncourt ◽  
...  
BMC Genomics ◽  
2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Katherine H. Tanaka ◽  
Antony T. Vincent ◽  
Jean-Guillaume Emond-Rheault ◽  
Marcin Adamczuk ◽  
Michel Frenette ◽  
...  

Vaccine ◽  
2013 ◽  
Vol 31 (45) ◽  
pp. 5256-5261 ◽  
Author(s):  
Philippe Vanden Bergh ◽  
Sarah E. Burr ◽  
Ottavia Benedicenti ◽  
Beat von Siebenthal ◽  
Joachim Frey ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33725 ◽  
Author(s):  
Katherine H. Tanaka ◽  
Stéphanie Dallaire-Dufresne ◽  
Rana K. Daher ◽  
Michel Frenette ◽  
Steve J. Charette

2020 ◽  
Vol 9 (1) ◽  
pp. 85
Author(s):  
Pierre-Étienne Marcoux ◽  
Antony T. Vincent ◽  
Marie-Ange Massicotte ◽  
Valérie E. Paquet ◽  
Émilie J. Doucet ◽  
...  

The type three secretion system (TTSS) locus of Aeromonas salmonicida subsp. salmonicida, located on the plasmid pAsa5, is known to be lost when the bacterium is grown at temperatures of 25 °C. The loss of the locus is due to the recombination of the insertion sequences flanking the TTSS region. However, the mechanism involved in this recombination is still elusive. Here, we analyzed 22 A. salmonicida subsp. salmonicida strains that had already lost their TTSS locus, and we systematically explored another 47 strains for their susceptibility to lose the same locus when grown at 25 °C. It appeared that strains from Europe were more prone to lose their TTSS locus compared to Canadian strains. More specifically, it was not possible to induce TTSS loss in Canadian strains that have AsaGEI2a, a genomic island, and prophage 3, or in Canadian strains without a genomic island. A comparative genomic approach revealed an almost perfect correlation between the presence of a cluster of genes, not yet characterized, and the susceptibility of various groups of strains to lose their locus. This cluster of genes encodes putative proteins with DNA binding capacity and phage proteins. This discovery creates new opportunities in the study of pAsa5 thermosensitivity.


2019 ◽  
Vol 25 (3) ◽  
Author(s):  
Mariano Larzábal ◽  
Hector A. Baldoni ◽  
Fernando D. Suvire ◽  
Lucrecia M. Curto ◽  
Gabriela E. Gomez ◽  
...  

2017 ◽  
Vol 85 (11) ◽  
Author(s):  
Einat Nissim-Eliraz ◽  
Eilam Nir ◽  
Irit Shoval ◽  
Noga Marsiano ◽  
Israel Nissan ◽  
...  

ABSTRACT Enteropathogenic Escherichia coli (EPEC) is a leading cause of severe intestinal disease and infant mortality in developing countries. Virulence is mediated by a type three secretion system (T3SS), causing the hallmark attaching and effacing (AE) lesions and actin-rich pedestal formation beneath the infecting bacteria on the apical surface of enterocytes. EPEC is a human-specific pathogen whose pathogenesis cannot be studied in animal models. We therefore established an EPEC infection model in human gut xenografts in SCID mice and used it to study the role of T3SS in the pathogenesis of the disease. Following EPEC O127:H6 strain E2348/69 infection, T3SS-dependent AE lesions and pedestals were demonstrated in all infected xenografts. We report here the development of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis in ∼50% of infected human gut xenografts. Using species-specific CD31 immunostaining, we showed that iTMA was limited to the larger human-mouse chimeric blood vessels, which are located between the muscularis mucosa and circular muscular layer of the human gut. These blood vessels were massively invaded by bacteria, which adhered to and formed pedestals on endothelial cells and aggregated with mouse neutrophils in the lumen. We conclude that endothelial infection, iTMA, and ischemic enteritis might be central mechanisms underlying severe EPEC-mediated disease.


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