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Tissue-Resident Type 2 Innate Lymphoid Cells Arrest Alveolarization in Bronchopulmonary Dysplasia
Journal of Immunology Research ( IF 4.1 ) Pub Date : 2020-10-31 , DOI: 10.1155/2020/8050186
Lanlan Mi 1 , Shaoxuan Zhu 1 , Jiayu Cai 1 , Suqing Xu 1 , Zhengyang Xue 1 , Hongyan Lu 1
Affiliation  

Bronchopulmonary dysplasia (BPD) is a severe complication of the respiratory system associated with preterm birth. Type 2 innate lymphoid cells (ILC2s) play a major role in tissue homeostasis, inflammation, and wound healing. However, the role in BPD remains unclear. The present study showed that ILC2s, interleukin-4 (IL-4), IL-13, and anti-inflammatory (M2) macrophages increased significantly in BPD mice as compared to the control mice. Administration with recombinant mouse IL-33 amplified the above phenomena and aggravated the alveolar structural disorder and functional injury in mice subjected to BPD, and the opposite was true with anti-ST2 antibody. In addition, the depletion of ILC2s in BPD mice with anti-CD90.2 antibody substantially abolished the destructive effect on BPD. In the treatment of BPD with dexamethasone, the number of ILC2s and M2 macrophages and levels of IL-4 and IL-13 decreased with remission as compared to the control group. This study identified a major destructive role of the ILC2s in BPD that could be attenuated as a therapeutic strategy.

中文翻译:

组织驻留的 2 型先天淋巴细胞阻止支气管肺发育不良肺泡化

支气管肺发育不良 (BPD) 是与早产相关的呼吸系统的严重并发症。2 型先天淋巴细胞 (ILC2) 在组织稳态、炎症和伤口愈合中起主要作用。然而,BPD 中的作用仍不清楚。本研究表明,与对照小鼠相比,BPD 小鼠的 ILC2、白细胞介素 4 (IL-4)、IL-13 和抗炎 (M2) 巨噬细胞显着增加。重组小鼠 IL-33 的给药放大了上述现象,加重了 BPD 小鼠的肺泡结构紊乱和功能损伤,而抗 ST2 抗体则相反。此外,用抗 CD90.2 抗体在 BPD 小鼠中消耗 ILC2s 基本上消除了对 BPD 的破坏作用。在用地塞米松治疗 BPD 时,与对照组相比,ILC2s和M2巨噬细胞的数量以及IL-4和IL-13的水平随着缓解而减少。这项研究确定了 ILC2s 在 BPD 中的主要破坏性作用,可以作为一种治疗策略减弱。
更新日期:2020-11-02
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