Jakab G J, Green G M
J Clin Invest. 1973 Nov;52(11):2878-84. doi: 10.1172/JCI107484.
Bacterial multiplication in the lung associated with murine Sendai virus pneumonia is caused by virus-induced defects in pulmonary bactericidal mechanisms. The nature of this effect has been studied in animals immunized against the challenge bacteria. Mice were immunized against Proteus mirabilis by intraperitoneal inoculation and by aerosol inhalation. After the development of immunity, mice were infected aerogenically with 10(4) TCID(50) of Sendai virus. 7 days later, during the height of the bronchial inflammation and pulmonary consolidation, the mice were challenged with an aerosol of viable (35)S-labeled Proteus mirabilis or (32)P-labeled Staphylococcus aureus.Nonimmunized virus-infected animals showed marked impairment of pulmonary bactericidal activity with subsequent multiplication of the bacterial strain in the case of Proteus mirabilis. Immunized nonvirus-infected animals showed enhancement of pulmonary bactericidal activity for the homologous and heterologous strains in comparison with nonimmunized animals. Virus-infected animals immunized by aerosol showed enhanced bactericidal activity against the homologous but not the heterologous bacterial strain. Neither virus infection nor immunization had a significant effect on the transport of particles in the lung. The data demonstrated that the bacterial multiplication associated with the virus pneumonia was prevented by preceding immunization against the homologous challenge organism. The data suggest a mechanism for controlling bacterial multiplication associated with virus pneumonias.
与鼠仙台病毒肺炎相关的肺部细菌繁殖是由病毒诱导的肺部杀菌机制缺陷引起的。这种效应的本质已在针对攻击细菌进行免疫的动物中进行了研究。通过腹腔接种和气溶胶吸入对小鼠进行奇异变形杆菌免疫。免疫形成后,小鼠经气溶胶感染10⁴组织培养感染剂量50(TCID₅₀)的仙台病毒。7天后,在支气管炎症和肺部实变高峰期,用活的³⁵S标记的奇异变形杆菌或³²P标记的金黄色葡萄球菌气溶胶攻击小鼠。未免疫的病毒感染动物肺部杀菌活性明显受损,随后奇异变形杆菌菌株繁殖。与未免疫动物相比,免疫的未病毒感染动物对同源和异源菌株的肺部杀菌活性增强。经气溶胶免疫的病毒感染动物对同源细菌菌株的杀菌活性增强,但对异源菌株则不然。病毒感染和免疫对肺部颗粒运输均无显著影响。数据表明,通过预先针对同源攻击生物体进行免疫可预防与病毒肺炎相关的细菌繁殖。这些数据提示了一种控制与病毒肺炎相关的细菌繁殖的机制。