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[肺结核患者中糖尿病与CD4+αβT细胞及单核细胞产生的γ干扰素、白细胞介素-12和白细胞介素-10之间的关系]

[The relation between diabetes mellitus and IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and monocytes in patients with pulmonary tuberculosis].

作者信息

Tsukaguchi K, Okamura H, Ikuno M, Kobayashi A, Fukuoka A, Takenaka H, Yamamoto C, Tokuyama T, Okamoto Y, Fu A, Yoshikawa M, Yoneda T, Narita N

机构信息

Second Department of Internal Medicine, Nara Medical University, Japan.

出版信息

Kekkaku. 1997 Nov;72(11):617-22.

PMID:9423299
Abstract

Diabetics are prone to bacterial infection in part, due to polymorphonuclear neutrophil dysfunction, but the precise mechanism is not yet fully explained. Of many complications, diabetes mellitus (DM) is one of the most common diseases, which causes pulmonary tuberculosis. To elucidate the mechanism of susceptibility to tuberculosis infection in patients with diabetes mellitus, we measured IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and autologous monocytes stimulated with live BCG in patients with pulmonary tuberculosis complicated with DM (TB + DM) or without DM (TB) and healthy controls. The levels of IFN-gamma and IL-12 production in TB patients were significantly lower than those in the control. These cytokine productions were also lower in TB + DM patients than in TB patients significantly. The level of IL-10 production in TB patients were highest among these three groups. The production of this cytokine in TB + DM patients was lowest. The level of IFN-gamma production was significantly lower in TB + DM patients under poor DM control than in those patients under good DM control and showed a significant negative correlation to HbA1c, an indicator of diabetic control. The period for negative conversion of culture finding in TB + DM patients under poor control was prolonged when compared with those in TB patients. These results demonstrated the difference in cytokines secretion profile between TB patients and TB + DM patients, and suggest that the immunological mechanism underlying pathogenesis of tuberculosis might work differently between these two patients groups.

摘要

糖尿病患者容易发生细菌感染,部分原因是多形核中性粒细胞功能障碍,但其确切机制尚未完全阐明。在众多并发症中,糖尿病(DM)是最常见的疾病之一,它会引发肺结核。为了阐明糖尿病患者易感染肺结核的机制,我们检测了肺结核合并糖尿病(TB + DM)或不合并糖尿病(TB)的患者以及健康对照者中,经活卡介苗刺激的CD4 + αβT细胞和自体单核细胞产生的干扰素-γ、白细胞介素-12和白细胞介素-10。肺结核患者中干扰素-γ和白细胞介素-12的产生水平显著低于对照组。这些细胞因子的产生在TB + DM患者中也明显低于肺结核患者。白细胞介素-10的产生水平在这三组中,肺结核患者最高。TB + DM患者中这种细胞因子的产生最低。在血糖控制不佳的TB + DM患者中,干扰素-γ的产生水平显著低于血糖控制良好的患者,并且与糖化血红蛋白(糖尿病控制的一个指标)呈显著负相关。与肺结核患者相比,控制不佳的TB + DM患者培养结果转阴的时间延长。这些结果表明了肺结核患者和TB + DM患者之间细胞因子分泌谱的差异,并提示这两组患者中肺结核发病机制的免疫机制可能有所不同。

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