ZFIN ID: ZDB-PUB-110609-18
Functional analysis of luxS in Streptococcus suis reveals a key role in biofilm formation and virulence
Wang, Y., Zhang, W., Wu, Z., Zhu, X., and Lu, C.
Date: 2011
Source: Veterinary Microbiology 152(1-2): 151-60 (Journal)
Registered Authors: Wang, Yang, Zhang, Wei
Keywords: Streptococcus suis; LuxS gene; Biofilm formation; Virulence
MeSH Terms: Animals; Bacterial Adhesion; Bacterial Proteins/genetics*; Biofilms*; Carbon-Sulfur Lyases/genetics* (all 17) expand
PubMed: 21621932 Full text @ Vet. Microbiol.
ABSTRACT
Streptococcus suis (SS) is an important pathogen of pigs, responsible for diverse diseases in swine and human. LuxS has been reported to play critical roles in both regulating various behaviors and interspecies quorum sensing in a large spectrum of bacteria. In this study, the luxS deletion mutant of SS was constructed using homologous recombination and its biofilm formation, hemolytic activity, cell adherence, virulence and expression of virulence factors were evaluated. Compared to the parental strain, the biofilm formation and hemolytic activity were significantly decreased in the luxS mutant. The addition of synthetic autoinducer 2 could complement the deficiencies of biofilm production in the mutant strain. Furthermore, its adherence to the HEp-2 cell line was dramatically decreased by 51% compared to the parental strain. Expressions of the known virulence genes gdh, cps, mrp, gapdh, sly, fbps and ef in the mutant strain were decreased by 0.66, 0.61, 0.45, 0.48, 0.29, 0.57 and 0.38, respectively, as quantified by real-time PCR. In a zebrafish infection model, the 50% lethal dose of the mutant strain was increased up to 10-fold. The findings demonstrated that the luxS gene deletion resulted in a significant decrease of bacterial biofilm formation, cell adhesion, hemolytic activity and transcription levels of many virulence genes in SS, and these factors may be associated with the attenuation of virulence in zebrafish. These results suggest that luxS may be involved in the interruption of bacterial communication and biofilm formation that contribute to the virulence of the bacterium.
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