Interleukin-17A Contributes to Bacterial Clearance in a Mouse Model of Streptococcal Toxic Shock-Like Syndrome.

Interleukin-17A Contributes to Bacterial Clearance in a Mouse Model of Streptococcal Toxic Shock-Like Syndrome.
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Interleukin-17A 有助于链球菌中毒性休克样综合征小鼠模型中的细菌清除

DOI:
10.3390/pathogens10060766
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发表时间:
2021-06-17
期刊:
Pathogens (Basel, Switzerland)
影响因子:
--
通讯作者:
Zhang AD
Zhang AD
中科院分区:
其他
文献类型:
--
作者:
Xu L;Lu X;Xiao P;Liu R;Xia KL;Wu MZ;Jin ML;Zhang AD

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猪链球菌(Streptococcus suis,S. suis)是一种新出现的人畜共患病原体,可引起人类链球菌中毒性休克样综合征(STSLS),死亡率高。STSLS的特征在于高细菌负荷、炎性细胞因子风暴、多器官功能障碍和最终的急性宿主死亡。虽然已经发现在STSLS发展过程中以NLRP 3依赖性方式诱导显著高水平的IL-17 A,但是IL-17 A对S.这一点还有待进一步阐明。在这项研究中,我们发现流行株SC 19比非流行株P17引起显著更高水平的IL-17 A。此外,从SC 19感染的il 17 a −/−小鼠中观察到的细菌负荷高于il 17 a +/+小鼠,尽管在两种类型的小鼠中均观察到急性死亡、组织损伤和炎性细胞因子风暴。此外,与il 17 a +/+小鼠相比,il 17 a −/−小鼠的中性粒细胞募集水平较低,诱导的抗菌蛋白质,如CRAMP,S100 A8和脂质运载蛋白-2的水平也在il 17 a −/−小鼠中降低。总之,本研究表明,IL-17 A不会导致严重的炎症,尽管它可能在STSLS期间通过诱导抗菌蛋白和促进中性粒细胞募集而对细菌清除起次要作用。
Streptococcus suis (S. suis), an emerging zoonotic pathogen, can cause streptococcal toxic shock-like syndrome (STSLS) in humans with high mortality. STSLS is characterized by high bacterial burden, an inflammatory cytokine storm, multi-organ dysfunction, and ultimately acute host death. Although it has been found that a significantly high level of IL-17A was induced in an NLRP3-dependent manner during STSLS development, the role of IL-17A on S. suis STSLS remains to be elucidated. In this study, we found that the epidemic strain SC 19 caused a significantly higher level of IL-17A than the non-epidemic strain P1/7. In addition, higher bacterial burden was observed from SC 19-infected il17a−/− mice than il17a+/+ mice, although acute death, tissue injury and inflammatory cytokines storm were observed in both types of mice. Furthermore, compared with il17a+/+ mice, the level of neutrophils recruitment was lower in il17a−/− mice, and the levels of induced antimicrobial proteins, such as CRAMP, S100A8 and lipocalin-2, were also decreased in il17a−/− mice. In conclusion, this study demonstrated that IL-17A does not contribute to the severe inflammation, although it may play a minor role for bacterial clearance by inducing antimicrobial proteins and promoting neutrophil recruitment during STSLS.
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