Ghigo Eric, Honstettre Amélie, Capo Christian, Gorvel Jean-Pierre, Raoult Didier, Mege Jean-Louis
Unite des Rickettsies, Unite Mixte de Recherche 6020 Centre National de la Recherche Scientifique, Universite de la Mediterranee, Institut Federatif de Recherche 48, Faculte de Medecine, Marseille, France.
J Infect Dis. 2004 Nov 15;190(10):1767-72. doi: 10.1086/425041. Epub 2004 Oct 7.
Q fever is caused by Coxiella burnetii, a bacterium that survives in monocytes/macrophages by resisting their natural microbicidal activity. Because the link between bacterial killing and phagosome maturation has yet to be demonstrated, we evaluated responses in monocytes from both immunologically naive control subjects and patients with various manifestations of Q fever. Monocytes from patients with chronic Q fever in evolution, who do not control the infection, exhibited defective phagosome maturation and impaired C. burnetii killing. Both responses were stimulated in patients recovering from Q fever. Phagosome maturation and C. burnetii killing were significantly correlated. Defective phagosome maturation and impaired C. burnetii killing were induced by adding interleukin (IL)-10 to monocytes from convalescent patients and were restored by IL-10 neutralization in chronic Q fever in evolution. We show that phagosome maturation and microbial killing are linked in Q fever and that IL-10 regulates both features of microbicidal activity.
Q热由贝纳柯克斯体引起，该细菌通过抵抗单核细胞/巨噬细胞的天然杀菌活性而在其中存活。由于细菌杀伤与吞噬体成熟之间的联系尚未得到证实，我们评估了免疫未接触过病原体的对照受试者以及患有各种Q热表现的患者单核细胞的反应。处于病情进展期、无法控制感染的慢性Q热患者的单核细胞表现出吞噬体成熟缺陷和贝纳柯克斯体杀伤受损。从Q热中恢复的患者这两种反应均受到刺激。吞噬体成熟与贝纳柯克斯体杀伤显著相关。向恢复期患者的单核细胞中添加白细胞介素（IL）-10可诱导吞噬体成熟缺陷和贝纳柯克斯体杀伤受损，而在病情进展期的慢性Q热中通过IL-10中和可使其恢复。我们表明，在Q热中吞噬体成熟与微生物杀伤相关联，并且IL-10调节杀菌活性的这两个特征。
