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肺部的炎症机制。

Inflammatory mechanisms in the lung.

机构信息

Department of Medicine, University of Louisville, Louisville, KY, USA, 40292.

出版信息

J Inflamm Res. 2009;2:1-11. Epub 2008 Dec 16.

PMID:22096348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3218724/
Abstract

Inflammation is the body's response to insults, which include infection, trauma, and hypersensitivity. The inflammatory response is complex and involves a variety of mechanisms to defend against pathogens and repair tissue. In the lung, inflammation is usually caused by pathogens or by exposure to toxins, pollutants, irritants, and allergens. During inflammation, numerous types of inflammatory cells are activated. Each releases cytokines and mediators to modify activities of other inflammatory cells. Orchestration of these cells and molecules leads to progression of inflammation. Clinically, acute inflammation is seen in pneumonia and acute respiratory distress syndrome (ARDS), whereas chronic inflammation is represented by asthma and chronic obstructive pulmonary disease (COPD). Because the lung is a vital organ for gas exchange, excessive inflammation can be life threatening. Because the lung is constantly exposed to harmful pathogens, an immediate and intense defense action (mainly inflammation) is required to eliminate the invaders as early as possible. A delicate balance between inflammation and anti-inflammation is essential for lung homeostasis. A full understanding of the underlying mechanisms is vital in the treatment of patients with lung inflammation. This review focuses on cellular and molecular aspects of lung inflammation during acute and chronic inflammatory states.

摘要

炎症是机体对各种损伤因素(包括感染、创伤和过敏)的反应。炎症反应十分复杂,涉及多种机制来抵御病原体并修复组织。在肺部,炎症通常由病原体或接触毒素、污染物、刺激物和过敏原引起。在炎症过程中,大量炎症细胞被激活。每个细胞释放细胞因子和介质,以改变其他炎症细胞的活性。这些细胞和分子的协调作用导致炎症的进展。临床上,急性炎症见于肺炎和急性呼吸窘迫综合征(ARDS),而慢性炎症表现为哮喘和慢性阻塞性肺疾病(COPD)。由于肺部是进行气体交换的重要器官,过度的炎症可能危及生命。由于肺部不断暴露于有害病原体,需要立即进行强烈的防御反应(主要是炎症),以尽早清除入侵物。炎症和抗炎之间的精细平衡对于肺稳态至关重要。充分了解潜在机制对于治疗肺部炎症患者至关重要。本综述重点介绍急性和慢性炎症状态下肺部炎症的细胞和分子方面。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1f/3218724/b73b23cd054b/jir-2-001f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1f/3218724/b73b23cd054b/jir-2-001f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1f/3218724/b73b23cd054b/jir-2-001f1.jpg

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