期刊
TOXINS
卷 13, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/toxins13010068
关键词
Staphylococcal toxins; toxic shock syndrome toxin 1; inflammasome; interleukin-1β
资金
- National Key Research and Development Program of China [2018YFD0500500]
- National Natural Science Foundation of China [31902256]
- Foundation for Innovation Research Group in Chongqing Universities [CXQT20004]
- earmarked fund for China Agriculture Research System [CARS37]
Staphylococcus aureus induces the expression of inflammatory cytokines in macrophages via the activation of the TLR4 and NLRP3 signaling pathways using its virulence factor TSST-1.
Staphylococcus aureus is a Gram-positive opportunistic pathogen which causes infections in a variety of vertebrates. Virulence factors are the main pathogenesis of S. aureus as a pathogen, which induce the host's innate and adaptive immune responses. Toxic shock syndrome toxin 1 (TSST-1) is one of the most important virulence factors of S. aureus. However, the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) in TSST-1-induced innate immune response is still unclear. Here, purified recombinant TSST-1 (rTSST-1) was prepared and used to stimulate mouse peritoneal macrophages. The results showed that under the action of adenosine-triphosphate (ATP), rTSST-1 significantly induced interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) production in mouse macrophages and the production was dose-dependent. In addition, rTSST-1+ATP-stimulated cytokine production in macrophage depends on the activation of toll like receptor 4 (TLR4), but not TLR2 on the cells. Furthermore, the macrophages of NLRP3(-/-) mice stimulated with rTSST-1+ATP showed significantly low levels of IL-1 beta production compared to that of wild-type mice. These results demonstrated that TSST-1 can induce the expression of inflammatory cytokines in macrophages via the activation of the TLR4 and NLRP3 signaling pathways. Our study provides new information about the mechanism of the TSST-1-inducing host's innate immune responses.
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