Background: Streptococcus suis type 2 (SS2) is an important zoonotic pathogen. We have previously reported the structure of LuxS protein and found that the luxS gene is closely related to biofilm, virulence gene expression and drug resistance of SS2. However, the mechanism of luxS mediated SS2 stress response is unclear. Therefore, this experiment performed stress response to luxS mutant (ΔluxS) and complement strain (CΔluxS), overexpression strain (luxS+) and wild-type SS2 strain HA9801, and analyzed the differential phenotypes in combination with transcriptome data.
Results: The results indicate that the luxS gene deletion causes a wide range of phenotypic changes, including chain length. RNA sequencing identified 278 lx-regulated genes, of which 179 were up-regulated and 99 were down-regulated. Differential genes focus on bacterial growth, stress response, metabolic mechanisms and drug tolerance. Multiple mitotic genes were down-regulated; while the ABC transporter system genes, cobalamin /Fe3+-iron carrier ABC transporter ATPase and oxidative stress regulators were up-regulated. The inactivation of the luxS gene caused a significant reduction in the growth and survival in the acid (pH = 3.0, 4.0, 5.0) and iron (100 mM iron chelator 2,2'-dipyridyl) stress environments. However, the mutant strain ΔluxS showed increased antioxidant activity to H2O2 (58.8 mmol/L).
Conclusions: The luxS gene in SS2 appears to play roles in iron metabolism and protective responses to acidic and oxidative environmental conditions.
Keywords: Acid resistance; Iron stress; Oxidative stress; Streptococcus suis; luxS gene.