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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Reactive oxygen species stimulated pulmonary epithelial cells mediate the alveolar recruitment of FasL + + killer B cells in LPS‐induced acute lung injuries
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Reactive oxygen species stimulated pulmonary epithelial cells mediate the alveolar recruitment of FasL + + killer B cells in LPS‐induced acute lung injuries

机译：反应性氧物种刺激肺上皮细胞介导的肺泡募集在LPS诱导的急性肺损伤中Fasl +杀伤B细胞的肺泡募集

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摘要

Abstract Reactive oxygen species (ROS) are electrophilic chemical species produced from incomplete oxidation. They have long been known as aggressive molecules that lead to direct tissue and cellular damage. Recent studies have reconsidered ROS as second messengers in the initiation and amplification of cell signaling, but how ROS regulate lung tissue and immune cell remain unknown. In this study, we used a LPS‐induced acute lung injury (ALI) mouse model to observe disease, progression and determine ROS‐related immune responses. We found that ROS play an essential pathogenic role in ALI, however, the major role of ROS in exacerbating ALI was increasing bronchoalveolar fluid (BALF) B cells rather than eliciting tissue damage. Moreover, these pathogenic B cells are FasL + killer B cells, which reported to damage Fas‐sensitive target cells including pulmonary epithelial cells. Furthermore, via in vitro transwell assays and in vivo treatment with neutralizing antibodies. ROS promoted pulmonary epithelial cells to produce CXCL9 and CXCL10, which recruited B cells into BALF. These results demonstrated that during lung injury, instead of causing oxidative damage, ROS mainly serve as second messengers, interacting with tissue and immune cells to enhance immune responses that lead to more severe disease.
机译：摘要反应性氧物质（ROS）是由不完全氧化产生的电子化学物质。它们长期以来被称为侵略性分子，导致组织和细胞损伤。最近的研究重新考虑了ROS作为第二信使在细胞信号传导的起始和扩增中的第二信使，但ROS调节肺组织和免疫细胞如何仍然未知。在这项研究中，我们使用LPS诱导的急性肺损伤（ALI）小鼠模型来观察疾病，进展和确定ROS相关的免疫反应。我们发现ROS在ALI中起重要的致病作用，然而，ROS在加剧ALI中的主要作用是增加支气管肺泡液（BALF）B细胞而不是引发组织损伤。此外，这些致病性B细胞是FasL +杀手B细胞，其报告用于损害包括肺上皮细胞的Fas敏感的靶细胞。此外，通过体外翻转测定和中和抗体的体内处理。 ROS促进肺上皮细胞以产生CXCL9和CXCL10，其将B细胞招募到BALF。这些结果表明，在肺损伤期间，ROS主要用作氧化损伤，而主要用作第二信使，与组织和免疫细胞相互作用，以增强导致更严重的免疫反应。

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