在临床上相关的肺部感染模型中,人类介质细胞阻碍了Mycobacterium avium的复制
Timothy D Shaw1, Anna D Krasnodembskaya1, Gunnar N Schroeder1
1Wellcome-Wolfson Institute for Experimental Medicine, Queen's University, Belfast, UK.
Thorax
|March 20, 2024
概括
人类介质细胞 (MSCs) 减少了巨细胞中的细胞内细菌和小鼠模型中的肺部感染Mycobacterium avium复杂肺病 (MAC-PD). 这种效应是由前列腺素E2 (PGE2) 信号传递的介导.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 微生物学 微生物学
背景情况:
- 对Mycobacterium avium复杂肺病 (MAC-PD) 需要新的治疗策略.
- 人类半机体 stromal 细胞 (MSCs) 显示出抑制MAC生长的潜力.
- MSCs对MAC-PD细胞内细菌的影响仍然未知.
研究的目的:
- 研究人类MSCs在感染MAC的巨细胞中减少细菌复制的能力.
- 评估MSCs对MAC感染巨细胞炎症的影响.
- 在MAC-PD的小鼠模型中评估MSCs的疗效.
主要方法:
- 人类单细胞衍生的巨细胞 (MDMs) 感染了Mycobacterium avium,并用人类骨髓衍生的MSCs进行治疗.
- 细菌殖民地形成单位 (CFU) 在细胞内和细胞外量化.
- 建立了MAC-PD的小鼠模型,并用MSC或盐水治疗小鼠,然后进行细菌和细胞因子分析.
主要成果:
- 在MDM中,MSCs减少了细胞内Mycobacterium avium的35% (p=0.027).
- 治疗MSC增加了前列腺素E2 (PGE2) 和降低瘤缩因子-α.
- 用MSC治疗的小鼠显示肺CFU减少了18% (p=0.012).
结论:
- MSCs调节炎症并通过COX-2/PGE2信号传递减少细胞内Mycobacterium avium在巨细胞中的生长.
- 在慢性MAC-PD的小鼠模型中,MSCs抑制了肺部细菌的复制.
- 这些发现凸显了MSC作为MAC-PD的潜在治疗策略.
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