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哮喘患者气道上皮细胞细胞因子释放对中性粒细胞凋亡的抑制作用及 S100A8、S100A9 的影响。

Suppressive effects of S100A8 and S100A9 on neutrophil apoptosis by cytokine release of human bronchial epithelial cells in asthma.

机构信息

Department of Senior Healthcare, BK21 Plus Program, Graduate School, Eulji University, Daejeon 34824.

Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan, 54538.

出版信息

Int J Med Sci. 2020 Feb 4;17(4):498-509. doi: 10.7150/ijms.37833. eCollection 2020.

DOI:10.7150/ijms.37833
PMID:32174780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7053304/
Abstract

S100A8 and S100A9 are important proteins in the pathogenesis of allergy. Asthma is an allergic lung disease, characterized by bronchial inflammation due to leukocytes, bronchoconstriction, and allergen-specific IgE. In this study, we examined the role of S100A8 and S100A9 in the interaction of cytokine release from bronchial epithelial cells, with constitutive apoptosis of neutrophils. S100A8 and S100A9 induce increased secretion of neutrophil survival cytokines such as MCP-1, IL-6 and IL-8. This secretion is suppressed by TLR4 inhibitor), LY294002, AKT inhibitor, PD98059, SB202190, SP600125, and BAY-11-7085. S100A8 and S100A9 also induce the phosphorylation of AKT, ERK, p38 MAPK and JNK, and activation of NF-κB, which were blocked after exposure to TLR4i, LY294002, AKTi, PD98059, SB202190 or SP600125. Furthermore, supernatants collected from bronchial epithelial cells after S100A8 and S100A9 stimulation suppressed the apoptosis of normal and asthmatic neutrophils. These inhibitory mechanisms are involved in suppression of caspase 9 and caspase 3 activation, and BAX expression. The degradation of MCL-1 and BCL-2 was also blocked by S100A8 and S100A9 stimulation. Essentially, neutrophil apoptosis was blocked by co-culture of normal and asthmatic neutrophils with BEAS-2B cells in the presence of S100A8 and S100A9. These findings will enable elucidation of asthma pathogenesis.

摘要

S100A8 和 S100A9 是过敏发病机制中的重要蛋白。哮喘是一种过敏性肺部疾病，其特征是白细胞引起的支气管炎症、支气管收缩和过敏原特异性 IgE。在这项研究中，我们研究了 S100A8 和 S100A9 在支气管上皮细胞细胞因子释放与中性粒细胞固有凋亡相互作用中的作用。S100A8 和 S100A9 诱导中性粒细胞存活细胞因子如 MCP-1、IL-6 和 IL-8 的分泌增加。这种分泌被 TLR4 抑制剂）、LY294002、AKT 抑制剂、PD98059、SB202190、SP600125 和 BAY-11-7085 抑制。S100A8 和 S100A9 还诱导 AKT、ERK、p38 MAPK 和 JNK 的磷酸化以及 NF-κB 的激活，这些激活在 TLR4i、LY294002、AKTi、PD98059、SB202190 或 SP600125 暴露后被阻断。此外，支气管上皮细胞在 S100A8 和 S100A9 刺激后收集的上清液抑制正常和哮喘中性粒细胞的凋亡。这些抑制机制涉及抑制半胱天冬酶 9 和半胱天冬酶 3 的激活以及 BAX 的表达。MCL-1 和 BCL-2 的降解也被 S100A8 和 S100A9 刺激阻断。基本上，S100A8 和 S100A9 的存在阻断了正常和哮喘中性粒细胞与 BEAS-2B 细胞的共培养中的中性粒细胞凋亡。这些发现将阐明哮喘的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c13b/7053304/e22453972eb6/ijmsv17p0498g013.jpg
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