LuxS/AI-2 in Streptococcus agalactiae reveals a key role in acid tolerance and virulence.

LuxS-mediated autoinducer-2 (AI-2) directly or indirectly regulates important physiologic function in a variety of bacteria. We found a luxS homologue in the genome of Streptococcus agalactiae, an important pathogen of tilapia. To investigate the relationship between luxS/AI-2 and pathogenicity for tilapia, its bioluminescent activity, acid resistance, cell adherence, virulence, and regulation of virulence gene were evaluated. Compared with the wild-type strain, the bioluminescent activity lost in the luxS mutant, its resistance to acid (pH2.8) was significantly decreased 33.8 times, and furthermore, its adherence to the NGF-2 cell line was dramatically reduced 3 times in the mutant strain. The virulence of the mutant strain was decreased in the tilapia infection model, exogenous AI-2 molecule (7.4nM) and luxS gene complementation with plasmid could complement the deficiencies of function in the luxS mutant strain. These results showed that inactivation of luxS gene caused a significant decrease of bioluminance, acid resistance, cell adhesion, virulence to tilapia and transcription levels of many virulence genes in S. agalactiae. Expression of the known stress resistance factors DnaK and GroEL, relative regulator factors CovR/CovS and virulence factor cpsE verified above results. These findings suggest that luxS may be involved in the interruption of bacterial virulence and resistance to environmental factors.