Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Department of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University & Beijing Institute of Respiratory Medicine, Beijing, China.
Cell Immunol. 2020 Jun;352:104098. doi: 10.1016/j.cellimm.2020.104098. Epub 2020 Mar 27.
Asthma is an inflammatory disease of the airways and numerous cytokines contribute to this pathogenesis. It is shown that challenge of airways with IL-33 induces asthma-like pathological changes in mice, but the possible downstream cytokines in this process remain to be characterised. To explore this, we compared changes in the airways of wildtype (WT) and IL-9 deficient mice challenged with IL-33. In line with previous report, per-nasal challenge of WT mice with IL-33 significantly increased the responsiveness of the airways along with infiltration of inflammatory cells, goblet cell hyperplasia, collagen deposition and smooth muscle hypertrophy, and the expression of cytokines compared with control group. Surprisingly, all of these pathological changes were significantly attenuated in IL-9 deficient mice following identical IL-33 challenge. These data suggest that IL-9 is one downstream cytokine relevant to the effects of IL-33 in asthmatic airways and consequently a potential therapeutic target for the treatment of asthma.
哮喘是一种气道炎症性疾病，许多细胞因子参与其发病机制。研究表明，IL-33 刺激气道可诱导小鼠产生类似哮喘的病理变化，但这一过程中可能的下游细胞因子仍有待鉴定。为了探讨这一问题，我们比较了 IL-33 刺激的野生型（WT）和 IL-9 缺陷型小鼠气道的变化。与之前的报道一致，与对照组相比，经鼻内给予 IL-33 刺激 WT 小鼠，可显著增加气道的反应性，同时伴有炎症细胞浸润、杯状细胞增生、胶原沉积和平滑肌肥大，以及细胞因子的表达增加。令人惊讶的是，在接受相同 IL-33 刺激后，IL-9 缺陷型小鼠的所有这些病理变化均明显减轻。这些数据表明，IL-9 是 IL-33 在哮喘气道中作用的下游细胞因子之一，因此可能是治疗哮喘的潜在治疗靶点。
