Ribosomal protein mediates Streptococcus suis serotype 2 virulence factor enolase to damage host cell mitochondria

Abstract:

[Background] Under normal physiological conditions, ribosomal protein SA is mainly expressed in cells and involved in a variety of cell functions. In the occurrence of infectious diseases, RPSA expresses in the cell membrane and mediates the infection of microorganisms. [Objective] To comprehensively reveal the role of RPSA in infection of hosts by Streptococcus suis serotype 2 (SS2). [Methods] The available cerebrospinal fluid and serum proteomics database (piglets with meningitis induced by SS2 and healthy piglets) was used, and bioinformatics methods were employed to screen the differentially expressed proteins (DEPs) in cerebrospinal fluid and serum and the involved signaling pathways were summarized. The host cells were stimulated by enolase (ENO) in vitro, and the changes of mitochondrial membrane potential, Ca²⁺ concentration, and reactive oxygen species were detected to reveal the effect of RPSA-mediated SS2-ENO on the main functions of the energy-generating organelle mitochondria in host cells. [Results] RPSA and related proteins were mainly enriched in energy-related pathways such as metabolism and glycolysis/gluconeogenesis after SS2 infection. SS2-ENO stimulation resulted in decreased mitochondrial membrane potential and increased Ca²⁺ level and ROS level in host cells. Blockade of RPSA alleviated the influence of ENO on mitochondrial membrane potential, ROS and Ca²⁺ concentration. [Conclusion] RPSA mediates the SS2 virulence factor ENO to damage host cell mitochondria. This study enriches the mechanism of RPSA in SS2 infection and provides a theoretical basis for the prevention and treatment of SS2 meningitis.