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肥大细胞介导铜绿假单胞菌脂多糖诱导的大鼠肺炎症。

Mast cells mediate Pseudomonas aeruginosa lipopolysaccharide-induced lung inflammation in rat.

机构信息

Peritox Laboratory, EA4285-UMI 01, Faculty of Medicine, Picardy Jules Verne University, 3 rue des Louvels, 80036, Amiens, France.

出版信息

Eur J Clin Microbiol Infect Dis. 2012 Aug;31(8):1983-90. doi: 10.1007/s10096-011-1530-5. Epub 2012 Jan 27.

Abstract

Activated mast cells have been demonstrated to play a pivotal role in Pseudomonas aeruginosa lung infections. However, there is no report about the involvement of mast cells in P. aeruginosa lipopolysaccharide (LPS)-induced lung inflammation. This study aimed at evaluating the role of mast cells in P. aeruginosa LPS-induced lung inflammation in rats. Mast cells stabilization was carried out by intraperitoneal injections of cromolyn. Lung inflammation was induced by the intratracheal instillation of P. aeruginosa LPS (5 μg/kg bw) and inflammatory status was evaluated 4 h post-LPS instillation. We found that activated mast cells could constitute a pivotal source of several inflammatory cytokines, including TNF-α, IL-1β, and IL-6. These cells might regulate polymorphonuclear neutrophil (PMN) recruitment and be implicated in the alteration of alveolar-capillary permeability via the release of TNF-α and IL-1β. We also detected that activated mast cells could be involved in the alteration of the expression of two epithelial tight junction proteins (claudin-1 and occludin) during the acute phase of inflammation. Our results suggest that activated mast cells might play a critical role in P. aeruginosa LPS-induced lung inflammation. Therefore, mast cell stabilization may be a potential novel approach for the prevention and treatment of P. aeruginosa-induced lung infections.

摘要

已证实活化的肥大细胞在铜绿假单胞菌肺部感染中发挥关键作用。然而,目前尚无关于肥大细胞参与铜绿假单胞菌脂多糖(LPS)诱导的肺部炎症的报道。本研究旨在评估肥大细胞在大鼠铜绿假单胞菌 LPS 诱导的肺部炎症中的作用。通过腹腔内注射色甘酸钠稳定肥大细胞。用铜绿假单胞菌 LPS(5μg/kg bw)经气管内滴注诱导肺部炎症,并在 LPS 滴注后 4 小时评估炎症状态。我们发现活化的肥大细胞可能是几种炎症细胞因子(包括 TNF-α、IL-1β 和 IL-6)的重要来源。这些细胞可能通过释放 TNF-α 和 IL-1β 来调节多形核中性粒细胞(PMN)的募集,并参与肺泡毛细血管通透性的改变。我们还发现,活化的肥大细胞可能参与了炎症急性期上皮细胞紧密连接蛋白(Claudin-1 和 Occludin)表达的改变。我们的结果表明,活化的肥大细胞可能在铜绿假单胞菌 LPS 诱导的肺部炎症中发挥关键作用。因此,肥大细胞稳定可能是预防和治疗铜绿假单胞菌感染引起的肺部感染的一种新的潜在方法。

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