IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.
IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.
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DOI：
10.1016/j.ebiom.2017.08.001
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发表时间：
2017-09
期刊：
影响因子：
11.1
通讯作者：
Ma L
中科院分区：
文献类型：
--
作者：
Hu S;He W;Du X;Yang J;Wen Q;Zhong XP;Ma L
据我们所知，没有研究检查中性粒细胞产生的IL-17在免疫防御结核分枝杆菌（MTB）感染和由MTB感染引起的类风湿关节炎（RA）的发病机制中的作用。在这里，我们确定了在结核分枝杆菌感染过程中，中性粒细胞以自分泌IL-6和IL-23依赖的方式表达IL-17。MT B H37 Rv诱导的IL-6产生依赖于NF-κB、p38和JNK信号通路;然而，IL-23产生依赖于中性粒细胞中的NF-κB和EKR。此外，我们发现Toll样受体2（TLR 2）和TLR 4介导了MTB H37 Rv感染的中性粒细胞中NF-κB、p38、ERK和JNK激酶的激活以及IL-6、IL-23和IL-17的产生。中性粒细胞产生的自分泌IL-17通过介导活性氧的产生和感染早期中性粒细胞的迁移，在抑制MTB H37 Rv生长中发挥重要作用。然而，中性粒细胞产生的IL-17在结核分枝杆菌感染期间促进胶原诱导的关节炎的发展。我们的研究结果确定了对分枝杆菌的保护机制和结核分枝杆菌在关节炎发展中的致病作用。在结核分枝杆菌感染过程中，中性粒细胞能够以依赖于自分泌IL-6和IL-23的方式表达IL-17。中性粒细胞自分泌IL-17在抑制结核分枝杆菌生长中起重要作用。结核分枝杆菌感染过程中中性粒细胞产生IL-17促进胶原诱导的关节炎发展
To our knowledge, no studies have examined the role of IL-17 production by neutrophils in immune defense against Mycobacterium tuberculosis (MTB) infection and the pathogenesis of rheumatoid arthritis (RA) caused by MTB infection. Here, we determined that neutrophils express IL-17 in an autocrine IL-6- and IL-23-dependent manner during MTB infection. MTB H37Rv-induced IL-6 production was dependent on the NF-κB, p38, and JNK signaling pathways; however, IL-23 production was dependent on NF-κB and EKR in neutrophils. Furthermore, we found that Toll-like receptor 2 (TLR2) and TLR4 mediated the activation of the kinases NF-κB, p38, ERK, and JNK and the production of IL-6, IL-23, and IL-17 in neutrophils infected with MTB H37Rv. Autocrine IL-17 produced by neutrophils played a vital role in inhibiting MTB H37Rv growth by mediating reactive oxygen species production and the migration of neutrophils in the early stages of infection. However, IL-17 production by neutrophils contributed to collagen-induced arthritis development during MTB infection. Our findings identify a protective mechanism against mycobacteria and the pathogenic role of MTB in arthritis development. Neutrophils were able to express IL-17 in a dependent on the autocrine IL-6 and IL-23 manner during Mycobacterium tuberculosis infection. Autocrine IL-17 in neutrophils played a vital role in inhibiting Mycobacterium tuberculosis growth. IL-17 production in neutrophils contributed to collagen-induced arthritis development during Mycobacterium tuberculosis infection.
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影响因子：
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作者：
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