Capo C, Zugun F, Stein A, Tardei G, Lepidi H, Raoult D, Mege J L
Unité des Rickettsies, Centre National de la Recherche Scientifique EPJ 0054, Marseille, France.
Infect Immun. 1996 May;64(5):1638-42. doi: 10.1128/iai.64.5.1638-1642.1996.
The occurrence of Q fever endocarditis likely involves some alterations in the responses of monocytes, the in vivo targets of Coxiella burnetii. To test this hypothesis, the production of the inflammatory cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 was assessed in monocytes from patients with Q fever endocarditis. Spontaneous transcription and secretion of tumor necrosis factor and interleukin-1 were significantly higher in patient monocytes than in healthy controls. The interleukin-6 transcripts were also upregulated in patient cells. Moreover, in patients with recent endocarditis exhibiting high titers of immunoglobulin G directed to C. burnetii in phase I, monocytes released significantly higher levels of tumor necrosis factor and interleukin-1 than in patients with stabilized endocarditis. Immunoglobulin G titers and the overproduction of tumor necrosis factor and interleukin-1 were significantly correlated. Hence, the overproduction of inflammatory cytokines might be a marker of disease activity.
Q热心内膜炎的发生可能涉及单核细胞（即伯氏考克斯体在体内的靶细胞）反应的某些改变。为验证这一假设，对Q热心内膜炎患者单核细胞中炎性细胞因子肿瘤坏死因子α、白细胞介素-1β和白细胞介素-6的产生情况进行了评估。患者单核细胞中肿瘤坏死因子和白细胞介素-1的自发转录和分泌显著高于健康对照。患者细胞中的白细胞介素-6转录物也上调。此外，在近期心内膜炎患者中，I期针对伯氏考克斯体的免疫球蛋白G滴度较高，其单核细胞释放的肿瘤坏死因子和白细胞介素-1水平显著高于病情稳定的心内膜炎患者。免疫球蛋白G滴度与肿瘤坏死因子和白细胞介素-1的过量产生显著相关。因此，炎性细胞因子的过量产生可能是疾病活动的一个标志物。
