Ghigo Eric, Imbert Guenièvre, Capo Christian, Raoult Didier, Mege Jean-Louis
Unité des Rickettsies, CNRS UMR 6020, IFR 48, Université de la Méditerranée, 13385 Marseille Cedex 05, France.
Ann N Y Acad Sci. 2003 Jun;990:450-9. doi: 10.1111/j.1749-6632.2003.tb07410.x.
Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic disease is characterized by impaired cell-mediated immune response and microbicidal activity of monocytes. We hypothesized that interleukin(IL)-4, a Th2 cytokine, interferes with the fate of C. burnetii inside monocytes. C. burnetii survived without multiplication in resting monocytes, but replicated in IL-4-treated monocytes. The effect of IL-4 is specific for monocytes since IL-4 did not stimulate C. burnetii replication in monocyte-derived macrophages. The effects of IL-4 on bacterial replication and on tumor necrosis factor (TNF) production in monocytes were apparently not related. Although IL-4 inhibited C. burnetii-stimulated release of TNF, the addition of recombinant TNF to IL-4-treated monocytes did not prevent the IL-4 effect. These results suggest that IL-4 enables monocytes to support C. burnetii replication and a Th2 polarization of immune response that may interfere with immune control of Q fever.
伯纳特立克次体是一种专性细胞内细菌，是Q热的病原体。这种慢性疾病的特征是细胞介导的免疫反应受损以及单核细胞的杀菌活性降低。我们推测白细胞介素（IL）-4（一种Th2细胞因子）会干扰伯纳特立克次体在单核细胞内的命运。伯纳特立克次体在静息单核细胞中存活但不繁殖，但在经IL-4处理的单核细胞中复制。IL-4的作用对单核细胞具有特异性，因为IL-4不会刺激源自单核细胞的巨噬细胞中伯纳特立克次体的复制。IL-4对单核细胞中细菌复制和肿瘤坏死因子（TNF）产生的影响显然没有关联。尽管IL-4抑制了伯纳特立克次体刺激的TNF释放，但向经IL-4处理的单核细胞中添加重组TNF并不能阻止IL-4的作用。这些结果表明，IL-4使单核细胞能够支持伯纳特立克次体的复制以及免疫反应的Th2极化，这可能会干扰Q热的免疫控制。
