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抗CCL2疗法减少了未成熟的肺部对氧的毒性

Tayyab Shahzad¹, Ying Dong¹, Nina K Behnke²

¹Department of General Pediatrics and Neonatology, Justus-Liebig-University and Universities of Giessen and Marburg Lung Center (UGMLC), German Lung Research Center (DZL), Feulgenstrasse 12, Giessen, Germany.

Cell death discovery

|July 3, 2024

概括

巨细胞的招募驱动了早产婴儿的支气管肺功能障碍症 (BPD). 在临床前模型中,阻断CCL-2有效降低了肺炎和损伤,为BPD提供了潜在的治疗方法.

科学领域:

新生儿医学新生儿医学
肺部病理学肺部病理学
免疫学免疫学免疫学

背景情况:

氧毒性是早产婴儿肺支气管发育不良症 (BPD) 的主要原因之一.
不成熟肺部的炎症反应,涉及细胞因子和免疫细胞,在BPD病变发生过程中至关重要.
迫切需要有效的疗法来缓解BPD中的肺炎.

研究的目的:

调查巨细胞在BPD病变发生中的作用.
评估阻断CCL-2的治疗潜力,以保护未成熟的肺部免受高氧损伤.

主要方法:

从早产婴儿 (<29周妊娠期) 的气管吸入物中分析了巨和中性粒细胞的概况.
使用CCL-2淘汰 (CCL-2-/-) 和暴露于高氧的野生型小鼠,具有或没有CCL-2阻断抗体.
评估肺炎,亡,细胞计数 (II型,介质干细胞,血管内皮细胞) 和肺形态学.

主要成果:

在婴儿中,CD14+CD16+巨细胞在第5天的较高比例与中度/严重的BPD有关.
暴露于高氧化的CCL-2-/-小鼠显示中性粒细胞的流入减少,亡减少,肺部结构保持.
野生型小鼠中CCL-2的治疗阻断模仿了这些保护作用,减少了炎症和肺损伤.

结论:

巨细胞的招募对BPD的发病有显著的贡献.
废除CCL-2功能代表了一种有前途的新疗法策略,以保护不成熟的肺部免受过氧损伤.

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