肺部压力变化的溶解气体引起人体外围血液中的免疫反应
Abigail G Harrell1, Stephen R Thom2, C Wyatt Shields1,3
1Department of Chemical and Biological Engineering, University of Colorado Boulder, Boulder, CO 80303, United States.
bioRxiv : the preprint server for biology
|October 31, 2023
概括
减压性疾病 (DCS) 可能源于免疫细胞对高气压的反应,而不仅仅是气泡. 这项研究揭示了在高压条件下的人类肺部模型中的免疫激活,这表明了DCS的新原因.
科学领域:
- 生理学 生理学 生理学
- 免疫学 免疫学 免疫学
- 生物医学工程 生物医学工程
背景情况:
- 传统理论将减压疾病 (DCS) 归因于气泡的形成,但气泡负载并不总是与症状严重程度相关.
- 这种差异表明有其他机制导致DCS病理,促使人们对压力下的细胞反应进行调查.
研究的目的:
- 为了研究一种假设,即溶解气体的部分压力升高会触发膜血管系统中免疫细胞的异常行为.
- 探索免疫细胞响应在解压疾病病因学中的作用.
主要方法:
- 使用了人类肺上芯片设备,使用初级气膜细胞和微血管细胞.
- 在正常或氧气减少的气膜气候条件下,压缩设备到1.0或3.5ATM.
- 进行了免疫细胞表型 (中性粒细胞,单细胞,树突细胞) 和多重ELISA.
主要成果:
- 在加压1小时内观察到免疫反应.
- 与氧气减少的空气相比,正常的气膜空气 (高压氧和) 诱导了更大的免疫细胞激活.
- 在高压条件下,特定的免疫细胞表型发生了改变.
结论:
- 溶解气体的部分压力升高,特别是在正常的膜空气中,似乎驱动了异常的免疫细胞表型.
- 在高压下,先天性免疫细胞反应被强烈认为是解压疾病 (DCS) 病因的促成因素.
- 这项研究挑战了以泡为中心的DCS观点,并强调了免疫系统在压力相关疾病中的作用.
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