Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences/Peking Union Medical College, Beijing 100730, China.
Department of Respiratory and Critical Care Medicine, China-Japan Friendship Hospital, Beijing 10029, China.
Aging (Albany NY). 2021 Sep 13;13(17):21729-21742. doi: 10.18632/aging.203515.
Asthma is driven by group 2 innate lymphoid cells, antigen-specific CD4+ T helper type 2 cells and their cytokines such as interleukin (IL)-4, IL-5, IL-13. IL-37 is decreased in asthma and negatively related to Th2 cytokines and other pro-inflammatory cytokines. Our study showed that IL-37 level in asthmatic peripheral blood mononuclear cells was lower than in healthy. Further, IL-37 was negatively correlated with exhaled nitric oxide, asthma control test score, atopy and rhinitis history in asthmatics. Then an OVA-induced asthma mice model treated with rhIL-37 was established. An antibody array was employed to uncover altered cytokines induced by IL-37 in mice lung tissue. 20 proteins differentially expressed after rhIL-37 treatment and five of them were validated in asthmatic peripheral blood mononuclear cells. Consistent with cytokine antibody array, CCL3, CCL4, CCL5 decreased after IL-37 administration. While CXCL9 and CXCL13 were no change. We concluded that IL-37 reduce asthmatic symptoms by inhibit pro-inflammatory cytokine such as CCL3, CCL4, CCL5.
哮喘是由 2 型固有淋巴细胞、抗原特异性 CD4+T 辅助型 2 细胞及其细胞因子（如白细胞介素（IL）-4、IL-5、IL-13）驱动的。哮喘患者的 IL-37 减少，与 Th2 细胞因子和其他促炎细胞因子呈负相关。我们的研究表明，哮喘患者外周血单个核细胞中的 IL-37 水平低于健康人。此外，IL-37 与哮喘患者呼出气一氧化氮、哮喘控制测试评分、特应性和鼻炎史呈负相关。然后建立了 rhIL-37 治疗的 OVA 诱导的哮喘小鼠模型。采用抗体阵列揭示 IL-37 诱导的小鼠肺组织中改变的细胞因子。rhIL-37 治疗后有 20 种蛋白质表达差异，其中 5 种在哮喘患者外周血单个核细胞中得到验证。与细胞因子抗体阵列一致，CCL3、CCL4、CCL5 在 IL-37 给药后减少，而 CXCL9 和 CXCL13 没有变化。我们得出结论，IL-37 通过抑制 CCL3、CCL4、CCL5 等促炎细胞因子来减轻哮喘症状。
