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Role of Immunity in Viral-Induced Bacterial Superinfections of the Lung

机译：免疫在病毒诱导的肺部细菌过度感染中的作用

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Although viral illnesses are predisposing causes for pulmonary bacterial infections, the interrelationships of viral virulence and host immunity to alterations in susceptibility to bacterial infection are incompletely understood. We used two mutant strains of encephalomyocarditis virus (minimally virulent Mengo-37A and a highly virulent Columbia SK [Col-SK]) to investigate these interrelationships. Mice that had been immunized to Mengo-37A, and nonimmunized controls, were challenged with aerosols containing 104 plaque-forming units of Mengo-37A or Col-SK per liter. The effect of each viral infection on pulmonary antibacterial activity was assessed 3 days later by measuring the capacity of the lungs to kill inhaled radiophosphorus (32P)-labeled Staphylococcus aureus. The degree of antibacterial dysfunction found was proportional to the virulence of the infecting virus. If the host was immune to the infecting virus, bactericidal function was not impaired by viral challenge. Neither mutant caused significant pulmonary damage; therefore: (i) viral-induced impairment in bactericidal activity reflects, quantitatively, the virulence of the virus and (ii) viral immunity protects pulmonary bacterial defenses by preventing damage to the phagocyte from the virus or its attendant metabolic abnormalities.
机译：尽管病毒性疾病是引起肺部细菌感染的诱因，但对病毒毒性和宿主免疫力对细菌感染易感性改变的相互关系还没有完全了解。我们使用了脑心肌炎病毒的两种突变株（最低毒性的Mengo-37A和高毒性的Columbia SK [Col-SK]）来研究这些相互关系。用每升含10 4 斑块形成的Mengo-37A或Col-SK的气雾剂对已经免疫过Mengo-37A和未免疫对照的小鼠进行攻击。 3天后，通过测量肺部杀死吸入的放射性磷（ 32 P）标记的金黄色葡萄球菌的能力，评估每种病毒感染对肺部抗菌活性的影响。发现的抗菌功能障碍的程度与感染病毒的毒力成正比。如果宿主对感染的病毒免疫，则病毒攻击不会削弱其杀菌功能。两种突变体均未引起明显的肺损伤。因此：（i）病毒引起的杀菌活性受损在数量上反映了病毒的毒性，并且（ii）病毒免疫通过防止病毒或其他伴随的代谢异常损害吞噬细胞来保护肺部细菌防御。

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