<i>pdh</i> modulate virulence through reducing stress tolerance and biofilm formation of <i>Streptococcus suis</i> serotype 2

Abstract

<i>Streptococcus suis</i> serotype 2 (<i>S. suis</i> 2) is a zoonotic pathogen. It causes meningitis, arthritis, pneumonia and sepsis in pigs, leading to extremely high mortality, which seriously affects public health and the development of the pig industry. Pyruvate dehydrogenase (PDH) is an important sugar metabolism enzyme that is widely present in microorganisms, mammals and higher plants. It catalyzes the irreversible oxidative decarboxylation of pyruvate to acetyl-CoA and reduces NAD+ to NADH. In this study, we found that the virulence of the <i>S. suis</i> ZY05719 sequence type 7 <i>pdh</i> deletion strain (Δ<i>pdh</i>) was significantly lower than the wild-type strain (WT) in the mouse infection model. The distribution of viable bacteria in the blood and organs of mice infected with the Δ<i>pdh</i> was significantly lower than those infected with WT. Bacterial survival rates were reduced in response to temperature stress, salt stress and oxidative stress. Additionally, compared to WT, the ability to adhere to and invade PK15 cells, biofilm formation and stress resistance of Δ<i>pdh</i> were significantly reduced. Moreover, real-time PCR results showed that <i>pdh</i> deletion reduced the expression of multiple adhesion-related genes. However, there was no significant difference in the correlation biological analysis between the complemented strain (CΔ<i>pdh</i>) and WT. Moreover, the survival rate of Δ<i>pdh</i> in RAW264.7 macrophages was significantly lower than that of the WT strain. This study shows that PDH is involved in the pathogenesis of <i>S. suis</i> 2 and reduction in virulence of Δ<i>pdh</i> may be related to the decreased ability to resist stress of the strain.