The airway epithelium: more than just a structural barrier.

The airway epithelium: more than just a structural barrier.
复制标题

DOI:
10.1177/1753465810396539
复制
发表时间:
2011-08-01
影响因子:
4.3
通讯作者:
Sin, Don D
Sin, Don D
中科院分区:
医学3区
文献类型:
--
作者:
Tam, Anthony;Wadsworth, Samuel;Sin, Don D

文献摘要

被引文献

相似文献

哺乳动物气道衬有各种专门的上皮细胞,这些细胞不仅可以用作物理屏障,而且还通过释放生物活性因子和持续的细胞更新来应对环境诱导的损害。通过分泌炎症介质和抗菌肽,以及通过将免疫细胞募集到感染或损害的部位,对肺上皮对环境损伤(例如病原体,香烟烟雾和污染)做出了反应。当上皮受到严重损害时,具有干细胞样性质的基底细胞和克拉拉细胞能够在受影响区域内自我更新和增殖,以修复损害。为了有效地抵抗感染,上皮需要通过跨内皮的外围循环中招募的中性粒细胞的帮助,然后进行跨层迁移事件。活化的中性粒细胞通过一系列配体 - 受体相互作用到损伤部位迁移到整个上皮,它们分泌蛋白水解酶,并将氧化自由基用于病原体破坏。然而,慢性阻塞性肺部疾病和哮喘等气道疾病中嗜中性粒细胞的慢性激活和募集与组织损伤和疾病严重程度有关。在本文中,我们回顾了对气道上皮反应的当前理解及其与炎症细胞的相互作用,尤其是中性粒细胞。
The mammalian airway is lined by a variety of specialized epithelial cells that not only serve as a physical barrier but also respond to environment-induced damage through the release of biologically active factors and constant cellular renewal. The lung epithelium responds to environmental insults such as pathogens, cigarette smoke and pollution by secreting inflammatory mediators and antimicrobial peptides, and by recruiting immune cells to the site of infection or damage. When the epithelium is severely damaged, basal cells and Clara cells that have stem-cell-like properties are capable of self-renewal and proliferation in the affected area, to repair the damage. In order to effectively fight off infections, the epithelium requires the assistance of neutrophils recruited from the peripheral circulation through transendothelial followed by transepithelial migration events. Activated neutrophils migrate across the epithelium through a series of ligand-receptor interactions to the site of injury, where they secrete proteolytic enzymes and oxidative radicals for pathogen destruction. However, chronic activation and recruitment of neutrophils in airway diseases such as chronic obstructive pulmonary disease and asthma has been associated with tissue damage and disease severity. In this paper, we review the current understanding of the airway epithelial response to injury and its interaction with inflammatory cells, in particular the neutrophil.