Hogg J C
University of British Columbia Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, Canada.
AJR Am J Roentgenol. 1994 Oct;163(4):769-75. doi: 10.2214/ajr.163.4.8092009.
Polymorphonuclear leukocytes (PMN) enter the circulation from the bone marrow and remain within the vascular space unless they become activated and migrate out of the vessels as part of an inflammatory response. This article reviews their behavior in the pulmonary circulation of both healthy and diseased individuals. First, the flow of PMN is compared with that of erythrocytes (RBC) to explain how differences in the traffic of these two cell types result in a concentration of PMN with respect to RBC in pulmonary capillary blood. Second, some recent concepts are presented concerning the role of PMN in the pathogenesis of emphysema, and the hypothesis is discussed that the inhalation of cigarette smoke contributes to the pathogenesis of emphysematous lung destruction by delaying and activating PMN while they travel through lung capillaries. Finally, the example of streptococcal (i.e., pneumococcal) pneumonia is used to illustrate new information as to how PMN adhere to the endothelium and migrate into an inflammatory site in the lung. The effect of this localized inflammatory response on PMN traffic in the surrounding lung also is discussed in relation to the pathogenesis of the generalized lung injury (acute respiratory disease syndrome [ARDS]) that can complicate severe pneumococcal lung infections.
多形核白细胞(PMN)从骨髓进入循环系统,并一直留在血管腔内,除非它们被激活并作为炎症反应的一部分迁移出血管。本文综述了它们在健康个体和患病个体肺循环中的行为。首先,将PMN的流动与红细胞(RBC)的流动进行比较,以解释这两种细胞类型在流量上的差异如何导致肺毛细血管血中PMN相对于RBC的浓度变化。其次,介绍了一些关于PMN在肺气肿发病机制中作用的最新概念,并讨论了一种假说,即吸入香烟烟雾通过在PMN穿过肺毛细血管时延迟并激活它们,从而促进肺气肿性肺破坏的发病。最后,以链球菌(即肺炎球菌)肺炎为例,说明关于PMN如何黏附于内皮并迁移到肺内炎症部位的新信息。还讨论了这种局部炎症反应对周围肺组织中PMN流量的影响,以及与可能使严重肺炎球菌肺部感染复杂化的全身性肺损伤(急性呼吸窘迫综合征[ARDS])发病机制的关系。