ATP Facilitates Staphylococcal Enterotoxin O Induced Neutrophil IL-1β Secretion via NLRP3 Inflammasome Dependent Pathways.

摘要: Staphylococcus aureus (S. aureus) is an important zoonotic food-borne pathogen causing severe invasive infections, such as sepsis, pneumonia, food poisoning, toxic shock syndrome and autoimmune diseases. Staphylococcal enterotoxin O (SEO) a new type of enterotoxins S. with superantigenic emetic activity. However, it still unclear about SEO-induced host inflammatory response. Therefore, the mechanism interleukin-1β (IL-1β) secretion in mouse neutrophils was investigated this study. Our results showed that recombinant SEO had activity high level gamma interferon (IFN-γ) production spleen cells induced cytokines expression including IL-1α, IL-1β, IL-6 TNF-α under action ATP. In addition, IL-1β dependent on activation Toll like receptor 4 (TLR4), nuclear factor kappa B (NF-κB) c-jun N-terminal kinase (JNK) signaling pathways. abolished NLRP3-/- mice compared those wild mice, indicating NLRP3 inflammasome mediated during stimulation Moreover, process SEO+ATP-induced potassium (K+) efflux. Taken together, our study suggests TLR4/JNK/NLRP3 pathway mediate maturation provides insight virulence factor-induced immune