Buret A, Dunkley M, Clancy R L, Cripps A W
Hunter Area Pathology Service, John Hunter Hospital, New Lambton Heights, New South Wales, Australia.
Infect Immun. 1993 Feb;61(2):671-9. doi: 10.1128/iai.61.2.671-679.1993.
This paper investigates the effector mechanisms of immune clearance in the lungs of rats immunized against mucoid Pseudomonas aeruginosa. After the gut-associated lymphoid tissue was primed and after a subsequent pulmonary challenge with live bacteria, significantly accelerated bacterial clearances from the lung and raised levels of anti-P. aeruginosa antibodies in sera (immunoglobulin G [IgG], IgA, and IgM) and bronchoalveolar lavages (IgG and IgA) were observed for all immune animals. These changes were associated with enhanced recruitment, chemotaxis, chemokinesis, phagocytic indices, and chemiluminescence of pulmonary polymorphonuclear neutrophils (PMN). In the alveolar spaces of immune animals, an increase in the level of PMN recruitment was not associated with higher levels of leukotriene B4 (LTB4). In contrast, in nonimmune animals that were intratracheally infected with P. aeruginosa, the levels of recruitment and activity of alveolar PMN were lower than those in immune rats but PMN infiltration correlated with a significant increase in the synthesis of LTB4 in the alveolar space. In pulmonary tissue, LTB4 synthesis for both groups was elevated. These findings suggest that accelerated clearance of mucoid P. aeruginosa from the lungs of intestinally immunized rats is due at least in part to factors that induce the enhancement of PMN recruitment and activity in the alveolar space. The mediators that regulate this enhanced response remain unknown but do not seem to include LTB4. The high levels of LTB4 measured in the bronchoalveolar lavages and pulmonary tissues from nonimmune animals infected with live bacteria implicate LTB4 as an important amplifier of the inflammatory response during acute pulmonary infections with mucoid P. aeruginosa in unimmunized hosts.
本文研究了针对黏液型铜绿假单胞菌免疫的大鼠肺部免疫清除的效应机制。在肠道相关淋巴组织被致敏后,以及随后用活细菌进行肺部攻击后,所有免疫动物的肺部细菌清除显著加速,血清(免疫球蛋白G [IgG]、IgA和IgM)和支气管肺泡灌洗液(IgG和IgA)中抗铜绿假单胞菌抗体水平升高。这些变化与肺多形核中性粒细胞(PMN)的募集增强、趋化性、化学增活现象、吞噬指数和化学发光有关。在免疫动物的肺泡腔中,PMN募集水平的增加与白三烯B4(LTB4)水平升高无关。相比之下,气管内感染铜绿假单胞菌的非免疫动物,肺泡PMN的募集和活性水平低于免疫大鼠,但PMN浸润与肺泡腔中LTB4合成的显著增加相关。在肺组织中,两组的LTB4合成均升高。这些发现表明,肠道免疫大鼠肺部黏液型铜绿假单胞菌清除加速至少部分归因于诱导肺泡腔中PMN募集和活性增强的因素。调节这种增强反应的介质尚不清楚,但似乎不包括LTB4。在感染活细菌的非免疫动物的支气管肺泡灌洗液和肺组织中测得的高LTB4水平表明,LTB4是未免疫宿主中黏液型铜绿假单胞菌急性肺部感染期间炎症反应的重要放大器。