Jakab G J, Green G M
Infect Immun. 1973 Jan;7(1):39-45. doi: 10.1128/iai.7.1.39-45.1973.
Many edemagenic and consolidating inflammatory diseases, such as virus pneumonias, of the lung are complicated by bacterial infection. Previous literature has stressed that edema and consolidation may promote bacterial proliferation by interfering with phagocytosis. To test that hypothesis, lung defense mechanisms were studied in guinea pigs with tuberculin-induced hypersensitivity pneumonitis, a noninfectious edemagenic, and consolidating inflammatory disease. Pulmonary bactericidal activity and particle clearance were measured with a mixed aerosol of (32)P-labeled Staphylococcus aureus and(35)S-labeled Proteus mirabilis. Hypersensitivity pneumonitis enhanced the bactericidal activity of the lung but had no effect on particle clearance despite the presence of consolidation and edema. These data indicate that altered host resistance to bacterial infection in acute inflammatory lung diseases can not be attributed to edema, inflammation, consolidation, changes in lung weight, etc., per se and that causes must be sought in functional changes in the bactericidal system of the lung rather than in specific histopathological changes.
许多导致水肿和实变的炎症性疾病，如病毒性肺炎，都会并发肺部细菌感染。以往文献强调，水肿和实变可能通过干扰吞噬作用促进细菌增殖。为验证这一假说，在患有结核菌素诱导的超敏性肺炎（一种非感染性的致水肿和实变的炎症性疾病）的豚鼠中研究了肺部防御机制。用含有³²P标记的金黄色葡萄球菌和³⁵S标记的奇异变形杆菌的混合气雾剂测量肺部杀菌活性和颗粒清除率。超敏性肺炎增强了肺部的杀菌活性，但尽管存在实变和水肿，对颗粒清除率却没有影响。这些数据表明，急性炎症性肺部疾病中宿主对细菌感染的抵抗力改变不能归因于水肿、炎症、实变、肺重量变化等本身，而必须在肺部杀菌系统的功能变化中寻找原因，而非特定的组织病理学变化。
