Acquiring high expression of suilysin enable non-epidemic Streptococccus suis to cause streptococcal toxic shock-like syndrome (STSLS) through NLRP3 inflammasome hyperactivation.
Acquiring high expression of suilysin enable non-epidemic Streptococccus suis to cause streptococcal toxic shock-like syndrome (STSLS) through NLRP3 inflammasome hyperactivation.
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Suilysin 的高表达使非流行性猪链球菌通过 NLRP3 炎症小体过度激活引起链球菌中毒性休克样综合征 (STSLS)
DOI：
10.1080/22221751.2021.1908098
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发表时间：
2021-12
影响因子：
13.2
通讯作者：
Zhang A
中科院分区：
文献类型：
--
作者：
Xu L;Lin L;Lu X;Xiao P;Liu R;Wu M;Jin M;Zhang A
摘要猪链球菌是近年来流行的猪链球菌病。猪溶血素（sulysin，SLY）基因是由非流行性猪溶血素（sulysin，SLY）基因的ST 1株逐步进化而来的。SLY的高表达是导致NLRP 3过度活化的必要条件，而NLRP 3过度活化是导致细胞因子风暴、多器官功能障碍和高死亡率的关键，是链球菌中毒性休克样综合征（STSLS）的特征。然而，由于基因组进化而获得高SLY表达是否足以使非流行性菌株引起STSLS仍有待阐明。在此，我们发现SLY在ST 1株（P1/7-SLY）中的过表达可以明显增加炎性小体的激活，这依赖于NLRP 3信号传导。相反，过表达突变体SLY（没有溶血活性的蛋白质）的菌株（P1/7-mSLY）不能显著增加炎性小体活化。此外，与流行株相似，P1/7-SLY可以在nlrp 3 +/+小鼠中引起STSLS，但在nlrp 3 −/−小鼠中不会。相比之下，P1/7-mSLY不能在nlrp 3 +/+小鼠和nlrp 3 −/−小鼠中引起STSLS。总之，我们证明了遗传进化使S。结论：SLY基因在猪源性大肠杆菌中的高表达可能是NLRP 3炎性小体过度活化的充分必要条件，而NLRP 3炎性小体过度活化可进一步导致细胞因子风暴和STSLS。
ABSTRACT The epidemic Streptococcus suis (S. suis) strain [Sequence type (ST) 7] was gradually evolving from the non-epidemic ST1 strain and got the ability for high expressing of suilysin (SLY). And the high expression of SLY was required for the epidemic strain to cause NLRP3 hyperactivation, which is essential for the induction of cytokines storm, dysfunction of multiple organs, and a high incidence of mortality, the characters of streptococcal toxic shock-like syndrome (STSLS). However, it remains to be elucidated whether acquiring high SLY expression due to genome evolution was sufficient for the non-epidemic strain to cause STSLS. Here, we found that the overexpression of SLY in ST1 strain (P1/7-SLY) could obviously increase the inflammasome activation, which was dependent on NLRP3 signalling. In contrast, the strain (P1/7-mSLY) overexpressing the mutant SLY (protein without hemolytic activity) could not significantly increase the inflammasome activation. Furthermore, similar to the epidemic strain, P1/7-SLY could cause STSLS in nlrp3 +/+ mice but not in nlrp3 −/− mice. In contrast, P1/7-mSLY could not cause STSLS in both nlrp3 +/+ mice and nlrp3 −/− mice. In summary, we demonstrate that genetic evolution enabling S. suis strain to express high level of SLY may be an essential and sufficient condition for NLRP3 inflammasome hyperactivation, which could further cause cytokines storm and STSLS.
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影响因子：
3.7
作者：
Chen C;Tang J;Dong W;Wang C;Feng Y;Wang J;Zheng F;Pan X;Liu D;Li M;Song Y;Zhu X;Sun H;Feng T;Guo Z;Ju A;Ge J;Dong Y;Sun W;Jiang Y;Wang J;Yan J;Yang H;Wang X;Gao GF;Yang R;Wang J;Yu J
通讯作者：
Yu J
Toll 样受体 4 赋予 Sulysin 炎症反应。
影响因子：
5.2
作者：
Bi L;Pian Y;Chen S;Ren Z;Liu P;Lv Q;Zheng Y;Zhang S;Hao H;Yuan Y;Jiang Y
通讯作者：
Jiang Y
影响因子：
11.8
作者：
Du P;Zheng H;Zhou J;Lan R;Ye C;Jing H;Jin D;Cui Z;Bai X;Liang J;Liu J;Xu L;Zhang W;Chen C;Xu J
通讯作者：
Xu J
影响因子：
5.2
作者：
Li G;Lu G;Qi Z;Li H;Wang L;Wang Y;Liu B;Niu X;Deng X;Wang J
通讯作者：
Wang J
影响因子：
3.3
作者：
Deng, Simin;Zhao, Liyang;Zhou, Rui
通讯作者：
Zhou, Rui