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首页> 外文期刊>Allergy >Pulmonary IL‐33 orchestrates innate immune cells to mediate respiratory syncytial virus‐evoked airway hyperreactivity and eosinophilia
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Pulmonary IL‐33 orchestrates innate immune cells to mediate respiratory syncytial virus‐evoked airway hyperreactivity and eosinophilia

机译：肺IL-33核对先天免疫细胞，以介导呼吸道合胞病毒诱发的气道高反应性和嗜酸性粒细胞症

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Abstract Background Respiratory syncytial virus (RSV) infection is epidemiologically linked to asthma. During RSV infection, IL‐33 is elevated and promotes immune cell activation, leading to the development of asthma. However, which immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clarified. We aimed to elucidate the individual roles of IL‐33‐activated innate immune cells, including ILC2s and ST2 + myeloid cells, in RSV infection‐triggered pathophysiology. Methods The role of IL‐33/ILC2 axis in RSV‐induced AHR inflammation and eosinophilia were evaluated in the IL‐33‐deficient and YetCre‐13 Rosa‐DTA mice. Myeloid‐specific, IL‐33‐deficient or ST2‐deficient mice were employed to examine the role of IL‐33 and ST2 signaling in myeloid cells. Results We found that IL‐33‐activated ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection. ILC2‐derived IL‐13 was sufficient for RSV‐driven AHR, since reconstitution of wild‐type ILC2 rescued RSV‐driven AHR in IL‐13‐deficient mice. Meanwhile, myeloid cell‐derived IL‐33 was required for airway inflammation, ST2 + myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL‐33 signaling in these cells. Local and peripheral eosinophilia is linked to both ILC2 and myeloid IL‐33 signaling. Conclusions This study highlights the importance of IL‐33‐activated ILC2s in mediating RSV‐triggered AHR and eosinophilia. In addition, IL‐33 signaling in myeloid cells is crucial for airway inflammation.
机译：摘要背景呼吸道同胞病毒（RSV）感染于流行性与哮喘有关。在RSV感染期间，IL-33升高并促进免疫细胞活化，导致哮喘的发育。然而，哪种免疫细胞负责触发气道过热（AHR），难以澄清炎症和嗜酸性粒细胞。我们的目标是在RSV感染触发的病理生理学中阐明IL-33活化的先天免疫细胞（包括ILC2S和ST2 +骨髓细胞）的个体作用。方法在IL-33缺陷和13 rosa-DTA小鼠中评估IL-33 / ILC2轴在RSV诱导的AHR炎症和嗜酸性粒细胞中的作用。使用霉菌特异性，IL-33缺陷或ST2缺陷小鼠检查IL-33和ST2信号传导在骨髓细胞中的作用。结果发现，在RSV感染期间，IL-33活化的ILC2S对于AHR和Airway炎症的开发至关重要。 ILC2衍生的IL-13足以用于RSV驱动的AHR，因为野生型ILC2重新构建了IL-13缺陷小鼠的RSV驱动的AHR。同时，气道炎症需要骨髓细胞衍生的IL-33，ST2 +骨髓细胞导致气道炎症的加剧，表明IL-33信号传导在这些细胞中的重要性。局部和外周嗜酸性粒细胞与ILC2和骨髓IL-33信号传导相关联。结论本研究突出了IL-33激活的ILC2S在介导RSV触发的AHR和嗜酸性粒细胞中的重要性。此外，骨髓细胞中的IL-33信号传导对气道炎症至关重要。

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