Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome.
Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome.
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中毒性休克综合征毒素 1 通过激活 NLRP3 炎性体诱导免疫反应
DOI：
10.3390/toxins13010068
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发表时间：
2021-01-18
期刊：
影响因子：
4.2
通讯作者：
Fang R
中科院分区：
文献类型：
--
作者：
Peng L;Jiang J;Chen T;Xu D;Hou F;Huang Q;Peng Y;Ye C;Hu DL;Fang R
金黄色葡萄球菌是一种革兰氏阳性机会致病菌，可引起多种脊椎动物感染。毒力因子是致病的主要因素。金黄色葡萄球菌作为病原体，其诱导宿主的先天性和适应性免疫应答。中毒性休克综合征毒素1（TSST-1）是沙门氏菌最重要的毒力因子之一。金黄色。然而，核苷酸结合寡聚化结构域样受体家族pyrin domain containing 3（NLRP 3）在TSST-1诱导的先天免疫应答中的作用仍不清楚。在此，制备纯化的重组TSST-1（rTSST-1）并用于刺激小鼠腹腔巨噬细胞。结果表明，rTSST-1在三磷酸腺苷（ATP）的作用下，可显著诱导小鼠巨噬细胞产生白细胞介素1β（IL-1β）和肿瘤坏死因子α（TNF-α），且呈剂量依赖性。此外，rTSST-1+ ATP刺激的巨噬细胞中细胞因子的产生依赖于细胞上Toll样受体4（TLR 4）的激活，而不是TLR 2。此外，与野生型小鼠相比，用rTSST-1+ATP刺激的NLRP 3 −/−小鼠的巨噬细胞显示出显著低水平的IL-1β产生。这些结果表明，TSST-1可以通过激活TLR 4和NLRP 3信号通路诱导巨噬细胞中炎性细胞因子的表达。我们的研究为TSST-1诱导宿主天然免疫反应的机制提供了新的信息。
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-1β (IL-1β) and tumor necrosis factor-α (TNF-α) 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-1β 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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影响因子：
3.7
作者：
McGilligan VE;Gregory-Ksander MS;Li D;Moore JE;Hodges RR;Gilmore MS;Moore TC;Dartt DA
通讯作者：
Dartt DA
影响因子：
5.5
作者：
Holzinger, Dirk;Gieldon, Laura;Loeffler, Bettina
通讯作者：
Loeffler, Bettina
影响因子：
6.7
作者：
Tuffs SW;James DBA;Bestebroer J;Richards AC;Goncheva MI;O'Shea M;Wee BA;Seo KS;Schlievert PM;Lengeling A;van Strijp JA;Torres VJ;Fitzgerald JR
通讯作者：
Fitzgerald JR
葡萄球菌肠毒素刺激T细胞刺激。克隆的可变响应和对附件或靶细胞上的主要组织相容性复合物II类分子的需求。
影响因子：
15.3
作者：
FLEISCHER, B;SCHREZENMEIER, H
通讯作者：
SCHREZENMEIER, H
影响因子：
2.3
作者：
Luhm, J;Kirchner, H;Rink, L
通讯作者：
Rink, L