Ansfield M J, Woods D E, Johanson W G
Infect Immun. 1977 Jul;17(1):195-204. doi: 10.1128/iai.17.1.195-204.1977.
We studied the bactericidal capacity of the rat lung during the development of pneumococcal pneumonia. Pneumonia was produced in a lower lobe by the intrabronchial instillation of 10(4)Streptococcus pneumoniae cells in buffer. Lung bacterial counts progressively increased, reaching 10(7) per lung within 48 h, and the increase was associated with localized atelectasis and consolidation. Bacterial multiplication was inhibited with tetracycline at various intervals after infection, and the subsequent clearance of pneumococci was determined. Viable pneumococci were rapidly killed by lung defenses if bacterial multiplication was inhibited within 12 h of the onset of infection. No change occurred in the bacterial populationif tetracycline was delayed until 24 h after infection, indicating that pneumococcal killing by lung defenses had ceased. This effect could be reproduced with the addition of pneumococcal capsular polysaccharide to the inoculum, which produced a dose-related inhibition of pneumococcal clearance. The clearance of S. epidermidis was not impaired in the presence of pneumococcal pneumonia or by administration of exogenous capsular polysaccharide. These data indicate that pneumococcal pneumonia causes a marked impairment in lung antipneumococcal defenses within 24 h of the onset of infection. This acquired defect in antibacterial defenses may be due to the accumulation of pneumococcal capsular material in the lungs of infected animals.
我们研究了肺炎球菌肺炎发展过程中大鼠肺的杀菌能力。通过在缓冲液中经支气管注入10⁴个肺炎链球菌细胞,在下叶诱发肺炎。肺细菌计数逐渐增加,48小时内每肺达到10⁷个,且这种增加与局限性肺不张和实变有关。在感染后的不同时间间隔用四环素抑制细菌繁殖,并测定随后肺炎球菌的清除情况。如果在感染开始后12小时内抑制细菌繁殖,存活的肺炎球菌会被肺防御机制迅速杀灭。如果四环素延迟至感染后24小时使用,则细菌数量无变化,这表明肺防御机制对肺炎球菌的杀灭作用已经停止。在接种物中添加肺炎球菌荚膜多糖可重现这种效应,其对肺炎球菌清除产生剂量相关的抑制作用。在存在肺炎球菌肺炎或给予外源性荚膜多糖的情况下,表皮葡萄球菌的清除不受影响。这些数据表明,肺炎球菌肺炎在感染开始后24小时内会导致肺抗肺炎球菌防御功能显著受损。这种获得性抗菌防御缺陷可能是由于感染动物肺中肺炎球菌荚膜物质的积累所致。