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2 型固有淋巴细胞在哮喘气道炎症中的作用。

The Involvement of Type 2 Innate Lymphoid Cells in Airway Inflammation of Asthma.

机构信息

Department of Pediatrics, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

出版信息

J Interferon Cytokine Res. 2020 Apr;40(4):188-194. doi: 10.1089/jir.2019.0180. Epub 2020 Mar 5.

DOI:10.1089/jir.2019.0180
PMID:32150691
Abstract

The airway inflammatory response is closely associated with asthma. The purpose of this article was to study the roles of innate lymphoid cells (ILCs) in the process of airway inflammatory response in asthma. We established the asthmatic mice model with intraperitoneal injected ovalbumin medium, then with the flow cytometry analysis, we detected the ILCs and their surface proteins in the mice blood samples, besides, we analyzed the amounts of inflammatory cytokines and secreted proteins in the mice bronchoalveolar lavage fluid and blood serum. Moreover, Western blot analyzed the proteins in the mice bronchial epithelial tissues. The ILC2 amounts were obviously increased in young asthmatic mice model. And, the proteins CD25 and CCR10 were highly expressed in the sorted ILC2s. Besides, the cytokines interleukin (IL)-5, IL-13, IL-33, CCL22, and CCL27 were abundant in the bronchoalveolar lavage fluid of asthmatic mice model. And, the secretion of IL-5, IL-13, IL-33, TSLP, and CCL22 in blood serum was much more in asthmatic mice model than in the normal control mice, whereas the secretion of PGD2 was suppressed in asthmatic mice bronchoalveolar lavage fluid and blood serum. Additionally, the guanine nucleotide-binding proteins Gα12 and Gα13 were upregulated in asthmatic mice bronchial tissues, and the protein SERCA2 was downregulated; moreover, the proteins NFAT, IRF4, and its downstream signal STAT6 were all upregulated in the asthmatic mice bronchial tissues. ILC2s were involved in the response of airway inflammation through secretion of proinflammatory cytokines and chemokines to dysregulate the Ca homeostasis in airway in the process of asthma. [Figure: see text].

摘要

气道炎症反应与哮喘密切相关。本文旨在研究固有淋巴细胞(ILC)在哮喘气道炎症反应过程中的作用。我们通过腹腔注射卵清蛋白建立哮喘小鼠模型,然后通过流式细胞术分析检测小鼠血液中的 ILC 及其表面蛋白,同时分析小鼠支气管肺泡灌洗液和血清中炎症细胞因子和分泌蛋白的含量。此外,Western blot 分析了小鼠支气管上皮组织中的蛋白。在幼年哮喘小鼠模型中,ILC2 的数量明显增加。并且,在分选的 ILC2 中高表达 CD25 和 CCR10 蛋白。此外,哮喘小鼠模型的支气管肺泡灌洗液中富含白细胞介素(IL)-5、IL-13、IL-33、CCL22 和 CCL27 等细胞因子。并且,哮喘小鼠模型血清中 IL-5、IL-13、IL-33、TSLP 和 CCL22 的分泌量明显多于正常对照组,而哮喘小鼠支气管肺泡灌洗液和血清中 PGD2 的分泌受到抑制。此外,哮喘小鼠支气管组织中 G 蛋白偶联蛋白 Gα12 和 Gα13 上调,钙结合蛋白 SERCA2 下调;而且,哮喘小鼠支气管组织中 NFAT、IRF4 及其下游信号 STAT6 蛋白均上调。ILC2 通过分泌促炎细胞因子和趋化因子参与气道炎症反应,从而在哮喘过程中调节气道钙稳态失衡。[图:见正文]。

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