ATP Facilitates Staphylococcal Enterotoxin O Induced Neutrophil IL-1β Secretion via NLRP3 Inflammasome Dependent Pathways.
ATP Facilitates Staphylococcal Enterotoxin O Induced Neutrophil IL-1β Secretion via NLRP3 Inflammasome Dependent Pathways.
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ATP 通过 NLRP3 炎症小体依赖性途径促进葡萄球菌肠毒素 O 诱导中性粒细胞 IL-1 β 分泌
DOI：
10.3389/fimmu.2021.649235
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发表时间：
2021
影响因子：
7.3
通讯作者：
Fang R
中科院分区：
文献类型：
--
作者：
Hou F;Peng L;Jiang J;Chen T;Xu D;Huang Q;Ye C;Peng Y;Hu DL;Fang R
金黄色葡萄球菌(S.aureus)是一种重要的人畜共患食源性致病菌，可引起严重的侵袭性感染，如败血症、肺炎、食物中毒、中毒性休克综合征和自身免疫性疾病等。金黄色葡萄球菌肠毒素O(SEO)是一种新型的金黄色葡萄球菌肠毒素，具有超抗原性和催吐活性。然而，SEO诱导的宿主炎症反应仍不清楚。因此，本研究探讨了SEO诱导小鼠中性粒细胞分泌IL-1β(IL-1β)的机制。结果表明，重组SEO具有超抗原活性，可在小鼠脾细胞中产生高水平的干扰素，并在γ作用下诱导炎性细胞因子IL-1α、IL-1β、IL-6和α在中性粒细胞中表达。此外，SEO诱导的IL-1β分泌依赖于Toll样受体4、核因子-kappaB和c-jun氨基末端激酶信号通路的激活。与野生型小鼠相比，NLRP3-/-小鼠中性粒细胞分泌IL-1β的能力减弱，提示在三磷酸腺苷作用下SEO刺激中性粒细胞时，NLRP3炎性小体的激活介导了中性粒细胞分泌IL-1β。此外，SEO+三磷酸腺苷诱导的IL-1β分泌过程依赖于K+外流。综上所述，我们的研究表明TLR4/JNK/NLRP3炎症体信号通路的激活介导了IL-1β的成熟和分泌，为金黄色葡萄球菌毒力因子诱导的宿主免疫应答提供了新的视角。
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) is a new type of enterotoxins of S. aureus with superantigenic and emetic activity. However, it is still unclear about SEO-induced host inflammatory response. Therefore, the mechanism of SEO-induced interleukin-1β (IL-1β) secretion in mouse neutrophils was investigated in this study. Our results showed that recombinant SEO had superantigenic activity with high level of gamma interferon (IFN-γ) production in mouse spleen cells and induced inflammatory cytokines expression including IL-1α, IL-1β, IL-6 and TNF-α in neutrophils under the action of ATP. In addition, SEO-induced IL-1β secretion was dependent on activation of Toll like receptor 4 (TLR4), nuclear factor kappa B (NF-κB) and c-jun N-terminal kinase (JNK) signaling pathways. However, SEO-induced IL-1β secretion was abolished in the neutrophils of NLRP3-/- mice compared with those of wild type mice, indicating that activation of NLRP3 inflammasome mediated IL-1β secretion during neutrophils stimulation with SEO under the action of ATP. Moreover, this process of SEO+ATP-induced IL-1β secretion was dependent on potassium (K+) efflux. Taken together, our study suggests that activation of TLR4/JNK/NLRP3 inflammasome signaling pathway mediate maturation and secretion of IL-1β and provides a new insight on S. aureus virulence factor-induced host immune response.
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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
DOI：
10.4049/jimmunol.1100381
发表时间：
2011-11-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Fang R;Tsuchiya K;Kawamura I;Shen Y;Hara H;Sakai S;Yamamoto T;Fernandes-Alnemri T;Yang R;Hernandez-Cuellar E;Dewamitta SR;Xu Y;Qu H;Alnemri ES;Mitsuyama M
通讯作者：
Mitsuyama M
影响因子：
5
作者：
Desouza, Ivani A.;Camargo, Enilton A.;Antunes, Edson
通讯作者：
Antunes, Edson
影响因子：
5.5
作者：
Krakauer, T
通讯作者：
Krakauer, T
影响因子：
7.3
作者：
Gombault A;Baron L;Couillin I
通讯作者：
Couillin I