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中性粒细胞会对感染呼吸道合胞病毒的呼吸道上皮细胞造成损伤。

Neutrophils induce damage to respiratory epithelial cells infected with respiratory syncytial virus.

作者信息

Wang S Z, Xu H, Wraith A, Bowden J J, Alpers J H, Forsyth K D

机构信息

Dept of Paediatrics, Flinders Medical Centre, Flinders University, SA, Australia.

出版信息

Eur Respir J. 1998 Sep;12(3):612-8. doi: 10.1183/09031936.98.12030612.

Abstract

The mechanisms by which respiratory syncytial virus (RSV) infection induces bronchiolitis and airway disease are unclear. The presence of large numbers of polymorphonuclear leukocytes (PMN) in the airways of infants with RSV infection suggests a potential role of PMN in airway injury associated with RSV infection. To investigate the potential role of neutrophils in RSV bronchiolitis, human alveolar type II cells (A549 cells) were infected with different doses of RSV for 6-48 h. A 51Cr-releasing assay was used to measure PMN-induced damage and image analysis was used to determine PMN adhesion and detachment of epithelial cells. The results showed that RSV infection of epithelial cells enhanced PMN adherence in a dose- and time-dependent pattern, RSV infection alone could damage and detach epithelial cells to a limited extent and PMN significantly augmented RSV infection-induced damage and detachment of epithelial cells. These data suggest that respiratory syncytial virus infection of respiratory epithelial cells enhances neutrophil adhesion to the epithelium and that activated neutrophils augment the damage and detachment of epithelium infected with the virus. Polymorphonuclear leukocytes may contribute to the pathogenesis of respiratory syncytial virus airway disease by inducing epithelial damage and cell loss.

摘要

呼吸道合胞病毒(RSV)感染诱发细支气管炎和气道疾病的机制尚不清楚。RSV感染婴儿气道中存在大量多形核白细胞(PMN),提示PMN在与RSV感染相关的气道损伤中可能发挥作用。为了研究中性粒细胞在RSV细支气管炎中的潜在作用,将人肺泡II型细胞(A549细胞)用不同剂量的RSV感染6 - 48小时。采用51Cr释放试验测量PMN诱导的损伤,并利用图像分析确定PMN对上皮细胞的黏附和脱离。结果显示,上皮细胞的RSV感染以剂量和时间依赖性方式增强PMN黏附,单独的RSV感染可在有限程度上损伤和使上皮细胞脱离,而PMN显著增强RSV感染诱导的上皮细胞损伤和脱离。这些数据表明,呼吸道上皮细胞的呼吸道合胞病毒感染增强中性粒细胞对上皮的黏附,并且活化的中性粒细胞加剧被病毒感染的上皮的损伤和脱离。多形核白细胞可能通过诱导上皮损伤和细胞丢失而参与呼吸道合胞病毒气道疾病的发病机制。

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