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IL-33 induced airways inflammation is partially dependent on IL-9.
Cellular Immunology ( IF 4.3 ) Pub Date : 2020-03-27 , DOI: 10.1016/j.cellimm.2020.104098
Xiaonan Du 1 , Chenduo Li 1 , Wenjun Wang 2 , Qiong Huang 1 , Jingjing Wang 3 , Zhaohui Tong 2 , Kewu Huang 2 , Yan Chen 1 , Huihui Yuan 1 , Zhe Lv 1 , Chris J Corrigan 4 , Wei Wang 1 , Sun Ying 1
Affiliation  

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.

中文翻译:

IL-33诱导的气道炎症部分取决于IL-9。

哮喘是气道的炎性疾病,许多细胞因子促成这种发病机理。结果显示,用IL-33攻击气道可在小鼠中诱发哮喘样病理变化,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)和受到IL-33攻击的IL-9缺陷小鼠气道的变化。与以前的报告一致,与对照组相比,WT-小鼠经鼻向IL-33的攻击显着增加了气道的反应性以及炎症细胞的浸润,杯状细胞增生,胶原蛋白沉积和平滑肌肥大,以及细胞因子的表达组。令人惊讶地,在相同的IL-33攻击后,在IL-9缺陷的小鼠中所有这些病理变化均被显着减弱。
更新日期:2020-03-28
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