An NLRP3 inflammasome-triggered cytokine storm contributes to Streptococcal toxic shock-like syndrome (STSLS)
Fig 7
Schematic representation of the mechanism underlying STSLS.
The present study indicated an important mechanism by which the epidemic S. suis strain causes STSLS. First, infection with S. suis can activate the transcription of genes involved in the inflammasome through pattern-recognition receptors, such as Toll-like receptor (TLR). Then, the high SLY expression level allows the strain to exert high levels of membrane perforation activity, which can further result in several events, including cytosolic K+ efflux, an essential event for NLRP3 inflammasome activation. Subsequently, the high level of inflammasome activation results in GSDMD, pro-IL-1β and pro-IL-18 cleavage, and the GSDMD cleavage leads to pyroptosis and facilitates secretion of mature IL-1β and IL-18, which may further induce the production of downstream cytokines, such as IFN-γ and IL-17A, causing a cytokine storm and multiple organ dysfunction, the main characteristics of STSLS.