Goldstein E, Bartlema H C
Bull Eur Physiopathol Respir. 1977 Jan-Feb;13(1):57-67.
This review concerns the role of the alveolar macrophage as part of the coordinated mucociliary, macrophge and immune bacterial defense mechanisms of the lung. Alveolar macrophages are end-stage phagocytes that are derived from two precursor sources; an uncommitted pleuripotential hematopoietic stem cell, and a committed differentiated pulmonary precursor which can renew itself, as well as mature into functional alveolar macrophages. Sufficient numbers of alveolar macrophages are distributed throughout the lungs to ensure their proximity to any bacteria that penetrates alveolar regions. Studies with rodents have shown that these alveolar macrophages ingest, inactivate, and degrade inhaled microorganisms within eight hours of their entrance into alveolar regions. The biochemical mechanisms responsible for this antibacterial function involve the elaboration of chemotactic factors consequent to the interaction of bacteria, antibody, and complement, and the presence of bactericidal substances within the macrophage itself. Normally, these cellular mechanisms enable the alveolar macrophage system to maintain the lungs bacteria-free. However, if macrophage function is impaired due to pollutant or viral exposure, the host-parasite balance is upset and bacterial proliferation ensues. In such circumstances, polymorphonuclear leucocytes and additional macrophages enter the area of bacterial proliferation to produce the classical inflammatory reaction of pneumonia.
本综述探讨了肺泡巨噬细胞作为肺部协调的黏液纤毛、巨噬细胞和免疫细菌防御机制一部分的作用。肺泡巨噬细胞是终末阶段的吞噬细胞,来源于两种前体来源;一种未定向的多能造血干细胞,以及一种定向分化的肺前体,它可以自我更新,并成熟为功能性肺泡巨噬细胞。足够数量的肺泡巨噬细胞分布在整个肺部,以确保它们接近任何穿透肺泡区域的细菌。对啮齿动物的研究表明,这些肺泡巨噬细胞在吸入的微生物进入肺泡区域后的八小时内将其摄取、灭活并降解。负责这种抗菌功能的生化机制包括细菌、抗体和补体相互作用后产生趋化因子,以及巨噬细胞本身内存在杀菌物质。正常情况下,这些细胞机制使肺泡巨噬细胞系统能够保持肺部无菌。然而,如果巨噬细胞功能因接触污染物或病毒而受损,宿主-寄生虫平衡就会被打破,细菌就会增殖。在这种情况下,多形核白细胞和额外的巨噬细胞进入细菌增殖区域,引发典型的肺炎炎症反应。