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阻断IL-17a信号减少肺炎和改善膜化在实验性支气管肺发育不良症

Meagan Goates¹, Amrit Shrestha¹, Shyam Thapa¹

¹Division of Neonatology, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.

The American journal of pathology

|August 8, 2024

概括

阻断炎症性细胞因子IL-17a可以减少小鼠bronchopulmonary dysplasia (BPD) 模型中的肺损伤. 这一发现表明IL-17a信号抑制可能是早产婴儿BPD的治疗策略.

科学领域:

新生儿免疫学新生儿免疫学
肺部医学肺部医学
炎症性疾病研究的研究.

背景情况:

支气管肺功能障碍症 (BPD) 是早产婴儿中普遍存在的慢性肺部疾病,经常导致长期健康问题.
炎症过程是导致BPD发展的关键因素.
亲炎性细胞因子IL-17a在BPD病变发生中的特定作用仍然在很大程度上是未知的.

研究的目的:

在新生小鼠中研究IL-17a在脂聚糖 (LPS) 诱导的实验性BPD中的作用.
确定阻断IL-17a信号是否可以减轻LPS介导的肺损伤和BPD发展.

主要方法:

新生野生型小鼠在囊性肺部阶段暴露在LPS或盐水中.
分析了肺部IL-17a表达和细胞来源 (包括γδT细胞).
在LPS暴露期间,小鼠接受了IL-17a阻断抗体或同型控制治疗.
肺部炎症标志物,膜化,血管化,细胞增殖和细胞亡被量化.

主要成果:

暴露于LPS会增加肺部IL-17a水平和IL-17a+,IL-22+细胞,主要来自γδ T细胞.
阻断IL-17a显著降低了LPS诱导的膜简化,亡,并抑制了细胞增殖.
与同型对照组相比,接受IL-17a阻断抗体治疗的LPS暴露小鼠的STAT1激活和IL-6水平较低.

结论:

在小鼠模型中,IL-17a信号封锁有效地减少了实验性BPD.
这些发现突出了IL-17a作为预防或治疗早产婴儿BPD的潜在治疗点.

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