Conventional dogma suggests that decompression sickness (DCS) is caused by nitrogen bubble nucleation in the blood vessels and/or tissues; however, the abundance of bubbles does not correlate with DCS severity. Since immune cells respond to chemical and environmental cues, we hypothesized that the elevated partial pressures of dissolved gases drive aberrant immune cell phenotypes in the alveolar vasculature. To test this hypothesis, we measured immune responses within human lung‐on‐a‐chip devices established with primary alveolar cells and microvascular cells. Devices were pressurized to 1.0 or 3.5 atm and surrounded by normal alveolar air or oxygen‐reduced air. Phenotyping of neutrophils, monocytes, and dendritic cells as well as multiplexed ELISA revealed that immune responses occur within 1 h and that normal alveolar air (i.e., hyperbaric oxygen and nitrogen) confer greater immune activation. This work strongly suggests innate immune cell reactions initiated at elevated partial pressures contribute to the etiology of DCS.

中文翻译：

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肺部压力变化产生的溶解气体会引起人体外周血的免疫反应

传统教条认为减压病 (DCS) 是由血管和/或组织中的氮气泡成核引起的；然而，气泡的丰富程度与 DCS 的严重程度无关。由于免疫细胞对化学和环境信号做出反应，我们假设溶解气体的分压升高会导致肺泡脉管系统中异常的免疫细胞表型。为了检验这一假设，我们测量了用原代肺泡细胞和微血管细胞建立的人肺芯片装置内的免疫反应。设备被加压至 1.0 或 3.5 atm，并被正常肺泡空气或低氧空气包围。中性粒细胞、单核细胞和树突状细胞的表型分析以及多重 ELISA 表明，免疫反应在 1 小时内发生，并且正常的肺泡空气（即高压氧和氮气）可赋予更大的免疫激活作用。这项工作强烈表明，在升高的分压下引发的先天免疫细胞反应有助于 DCS 的病因学。