Kirby Alun C, Raynes John G, Kaye Paul M
Immunology Unit, Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom.
J Infect Dis. 2006 Jan 15;193(2):205-13. doi: 10.1086/498874. Epub 2005 Dec 1.
Despite their close physical and functional relationships, alveolar macrophages (AMs) and pulmonary dendritic cells (pulDCs) have rarely been examined together in the context of infection. Using a nonlethal, resolving model of pneumonia caused by intranasal injection of Streptococcus pneumoniae, we demonstrate that AMs and pulDCs exhibit distinct characteristics during pulmonary inflammation. Recruitment of AMs and pulDCs occurred with different kinetics, and increased numbers of AMs resulted mainly from the appearance of a distinct subset of CD11b(High) AMs. Increased numbers of CD11b(High) and CD11b(Low) AMs, but not pulDCs, were recoverable from bronchoalveolar lavage fluid. CD11b expression on AMs was significantly increased by granulocyte-macrophage colony-stimulating factor but not by interleukin-10 or pathogen-associated stimuli. Finally, antibody blockade demonstrated that CD11b was critical for the recruitment of AMs, but not pulDCs, into the lung after pneumococcal challenge. These data demonstrate that there are significant differences between AM and pulDC responses to inflammatory pathogenic stimuli in vivo.
尽管肺泡巨噬细胞(AMs)和肺树突状细胞(pulDCs)在物理和功能上关系密切,但在感染情况下很少同时对它们进行研究。我们采用鼻内注射肺炎链球菌所致的非致死性、可消退的肺炎模型,证明AMs和pulDCs在肺部炎症过程中表现出不同的特征。AMs和pulDCs的募集动力学不同,AMs数量增加主要源于出现了一个独特的CD11b(高)AMs亚群。从支气管肺泡灌洗液中可回收数量增加的CD11b(高)和CD11b(低)AMs,但无法回收pulDCs。粒细胞-巨噬细胞集落刺激因子可显著增加AMs上CD11b的表达,但白细胞介素-10或病原体相关刺激则无此作用。最后,抗体阻断实验表明,CD11b对肺炎球菌攻击后AMs募集到肺中至关重要,但对pulDCs募集并非如此。这些数据表明,AMs和pulDCs在体内对炎症致病刺激的反应存在显著差异。