Regulation of experimental lung inflammation

Alex B Lentsch , Peter A Ward
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引用次数: 79

Abstract

Acute lung inflammation is an important component of a number of pulmonary diseases, including acute respiratory distress syndrome (ARDS). Much has been learned about the manner in which various insults to lung, such as infection or trauma, bring about recruitment of neutrophils into alveoli and small airways, resulting in parenchymal damage and organ dysfunction. In this brief review, we discuss the endogenous mechanisms in which the lung regulates the acute inflammatory response in rats to intrapulmonary deposition of IgG immune complexes. Emphasis is given to the participation of the transcription factor, NF-κB, in the development of lung injury and the endogenous mediators which attempt to control the extent of lung inflammation by modulating the activation of NF-κB.

实验性肺炎症的调节
急性肺部炎症是包括急性呼吸窘迫综合征(ARDS)在内的许多肺部疾病的重要组成部分。关于各种肺部损伤,如感染或创伤,导致嗜中性粒细胞聚集到肺泡和小气道,导致实质损伤和器官功能障碍的方式,我们已经了解了很多。在这篇简短的综述中,我们讨论了肺调节大鼠对肺内IgG免疫复合物沉积的急性炎症反应的内源性机制。重点是转录因子NF-κB在肺损伤发展中的参与,以及试图通过调节NF-κB的激活来控制肺部炎症程度的内源性介质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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