Capo C, Zaffran Y, Zugun F, Houpikian P, Raoult D, Mege J L
Unité des Rickettsies, Centre National de la Recherche Scientifique UPRES A, Faculté de Médecine, Marseille, France.
Infect Immun. 1996 Oct;64(10):4143-7. doi: 10.1128/iai.64.10.4143-4147.1996.
The pathophysiology of Q fever endocarditis is characterized by the suppression of antigen-specific cell-mediated immune responses. We investigated the production of interleukin-10 (IL-10) and transforming growth factor beta (TGF-beta), known to interfere with the development of protective cell immunity. IL-10 was markedly released by unstimulated peripheral blood mononuclear cells (PBMC) from patients with Q fever endocarditis. This release resulted from the upregulation of IL-10 gene transcription. Similarly, the release of TGF-beta1 and TGF-beta2 was significantly higher in patient PBMC than in control cells, but the expression of their respective mRNA was not enhanced in patient cells. In contrast, lipopolysaccharide-stimulated transcription and release of IL-10 and TGF-beta were similar in patients and controls. The release of IL-10 by PBMC but not that of TGF-beta was correlated with the clinical status of the patients. First, IL-10 production was correlated with specific antibody levels. Second, IL-10 release remained elevated in patients prone to relapse. Taken together, our results suggest that the release of IL-10 and TGF-beta is upregulated in Q fever endocarditis. IL-10 might be considered as a marker of disease relapses and might be instrumental in monitoring the efficiency of the treatment.
Q热心内膜炎的病理生理学特征是抗原特异性细胞介导免疫反应受到抑制。我们研究了已知会干扰保护性细胞免疫发展的白细胞介素-10（IL-10）和转化生长因子β（TGF-β）的产生。Q热心内膜炎患者未受刺激的外周血单核细胞（PBMC）可显著释放IL-10。这种释放是由IL-10基因转录上调所致。同样，患者PBMC中TGF-β1和TGF-β2的释放明显高于对照细胞，但其各自mRNA的表达在患者细胞中并未增强。相反，脂多糖刺激后，患者和对照中IL-10和TGF-β的转录及释放相似。PBMC释放IL-10而非TGF-β与患者的临床状况相关。首先，IL-10的产生与特异性抗体水平相关。其次，易复发患者的IL-10释放仍处于较高水平。综上所述，我们的结果表明，Q热心内膜炎中IL-10和TGF-β的释放上调。IL-10可被视为疾病复发的标志物，可能有助于监测治疗效果。
