Disruption of srtA gene in Streptococcus suis results in decreased interactions with endothelial cells and extracellular matrix proteins.

Abstract	Streptococcus suis, a major pathogen of swine, is an emerging zoonotic agent which causes meningitis and septic shock. In this study, we investigated the ability of S. suis mutant strain (SRTDeltaA) lacking the sortase A gene (srtA) to interact with host cells and extracellular matrix (ECM) proteins, as well as its virulence in a mouse infection model. We demonstrated that mutant SRTDeltaA had reduced capacity to adhere to and invade porcine brain microvascular endothelial cells compared to the wild-type strain. In addition, mutant SRTDeltaA also showed significantly less adherence to plasma fibronectin, cellular fibronectin and collagen type I. However, disruption of srtA had little effect on the virulence of S. suis in a mouse intraperitoneal model of infection. These results indicate that surface proteins anchored by sortase A are required for a normal level of bacterial binding. However, other factors may also be important for S. suis virulence and interaction with host tissues.
Authors	G Vanier, T Sekizaki, M C Domínguez-Punaro, M Esgleas, M Osaki, D Takamatsu, M Segura, M Gottschalk
Journal	Veterinary microbiology (Vet Microbiol) Vol. 127 Issue 3-4 Pg. 417-24 (Mar 18 2008) ISSN: 0378-1135 [Print] Netherlands
PMID	17954016 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Bacterial Proteins Extracellular Matrix Proteins Fibronectins Collagen Aminoacyltransferases sortase A Cysteine Endopeptidases
Topics	Aminoacyltransferases (genetics) Animals Bacterial Adhesion (physiology) Bacterial Proteins (genetics, metabolism) Cell Line Cells, Cultured Collagen (metabolism) Cysteine Endopeptidases (genetics) Disease Models, Animal Endothelial Cells (microbiology) Extracellular Matrix Proteins (metabolism) Female Fibronectins (metabolism) Humans Mice Mice, Inbred Strains Mutation Protein Binding Streptococcal Infections (microbiology) Streptococcus suis (genetics, pathogenicity, physiology) Swine Virulence (physiology)

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