Reuter Helmuth, Burgess Lesley J, Carstens Machteld E, Doubell Anton F
Cardiology Unit/TREAD Research, P.O. Box 19174, Tygerberg 7505, South Africa.
Tuberculosis (Edinb). 2006 Mar;86(2):125-33. doi: 10.1016/j.tube.2005.08.018. Epub 2005 Dec 19.
To investigate the immunopathogenesis of pericardial tuberculosis (TB) and the influence of human immunodeficiency virus (HIV) on the anti-tuberculous immune response.
Consecutive patients presenting with large pericardial effusions were subjected to a full clinical examination and pericardiocentesis. Aspirated fluid was sent for biochemistry, differential leukocyte count, flow cytometric analysis and determination of cytokine levels. Pericardial tissue was sent for TB culture and histopathological evaluation. Diagnoses were made according to pre-determined criteria.
Fifty-six patients were included and divided into HIV positive TB (n = 22), HIV negative TB (n = 21) and non-tuberculous effusions (n = 13). Peripheral blood neutrophil, lymphocyte and monocyte counts were significantly lower in HIV positive TB patients. Lymphocytes were the dominant cell type in tuberculous pericardial effusions. CD4+ cells dominated in HIV negative tuberculous effusions, whereas CD8+ cells dominated in HIV positive TB. The difference in the concentration of IFN-gamma levels in the tuberculous and non-tuberculous pericardial effusions was statistically significant. Despite significant differences in pericardial CD4+ cell counts, IFN-gamma levels were similarly elevated in HIV negative and HIV positive tuberculous effusions. Highest levels of pericardial IL-10 were observed in samples associated with least tissue necrosis, suggesting the possibility of a tissue protective immunoregulatory role for IL-10.
Tuberculous pericardial effusions result from a T helper1 (Th1)-dominant immune response. IFN-gamma producing CD4+ lymphocytes dominate in HIV negative patients, whereas CD8+ seem to play a more important role in HIV positive patients. Infection with HIV leads to the depletion of immunocompetent cells such as monocytes, NK cells and neutrophils.
探讨心包结核（TB）的免疫发病机制以及人类免疫缺陷病毒（HIV）对抗结核免疫反应的影响。
对连续出现大量心包积液的患者进行全面临床检查及心包穿刺术。抽取的液体送去进行生化检查、白细胞分类计数、流式细胞术分析及细胞因子水平测定。心包组织送去进行结核菌培养及组织病理学评估。根据预先确定的标准做出诊断。
纳入56例患者，分为HIV阳性结核组（n = 22）、HIV阴性结核组（n = 21）和非结核性积液组（n = 13）。HIV阳性结核患者外周血中性粒细胞、淋巴细胞和单核细胞计数显著降低。淋巴细胞是结核性心包积液中的主要细胞类型。CD4+细胞在HIV阴性结核性积液中占主导，而CD8+细胞在HIV阳性结核中占主导。结核性和非结核性心包积液中IFN-γ水平的浓度差异具有统计学意义。尽管心包CD4+细胞计数存在显著差异，但HIV阴性和HIV阳性结核性积液中的IFN-γ水平同样升高。在心包组织坏死最少的样本中观察到最高水平的心包IL-10，提示IL-10可能具有组织保护免疫调节作用。
结核性心包积液由以辅助性T细胞1（Th1）为主导的免疫反应引起。产生IFN-γ的CD4+淋巴细胞在HIV阴性患者中占主导，而CD8+细胞在HIV阳性患者中似乎发挥更重要的作用。HIV感染导致免疫活性细胞如单核细胞、NK细胞和中性粒细胞耗竭。
