IL-33 induced airways inflammation is partially dependent on IL-9
IL-33 induced airways inflammation is partially dependent on IL-9
复制标题
IL-33 诱导的气道炎症部分依赖于 IL-9
DOI：
10.1016/j.cellimm.2020.104098
复制
发表时间：
2020-06-01
影响因子：
4.3
通讯作者：
Ying, Sun
中科院分区：
文献类型：
--
作者：
Du, Xiaonan;Li, Chenduo;Ying, Sun
哮喘是一种气道炎症性疾病，许多细胞因子参与了哮喘的发病机制。结果表明，用IL-33攻击气道诱导小鼠哮喘样病理变化，但该过程中可能的下游细胞因子仍有待表征。为了探索这一点，我们比较了野生型（WT）和IL-9缺陷小鼠用IL-33激发的气道变化。与先前的报道一致，与对照组相比，用IL-33经鼻激发WT小鼠显著增加气道的反应性沿着炎性细胞浸润、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。令人惊讶的是，在相同的IL-33攻击后，所有这些病理变化在IL-9缺陷小鼠中显著减弱。这些数据表明，IL-9是一个下游细胞因子相关的IL-33在哮喘气道的作用，因此，一个潜在的治疗哮喘的治疗目标。
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.