The pro-inflammatory effect of Staphylokinase contributes to community-associated Staphylococcus aureus pneumonia.

ABSTRACT: Pneumonia caused by community-associated Staphylococcus aureus (CA-SA) has high morbidity and mortality, but its pathogenic mechanism remains to be further investigated. Herein, we identify that staphylokinase (SAK) is significantly induced in CA-SA and inhibits biofilm formation in a plasminogen-dependent manner. Importantly, SAK can enhance CA-SA-mediated pneumonia in both wild-type and cathelicidins-related antimicrobial peptide knockout (CRAMP^-/-) mice, suggesting that SAK exacerbates pneumonia in a CRAMP-independent manner. Mechanistically, SAK induces pro-inflammatory effects, especially in the priming step of NLRP3 inflammasome activation. Moreover, we demonstrate that SAK can increase K⁺ efflux, production of reactive oxygen species production, and activation

SUBMITTER: Wang Y 

PROVIDER: S-EPMC9226170 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature