Sharifabadi Abumoslem Rashidi, Hassanshahi Gholamhossein, Ghalebi Seyed Razi, Arababadi Mohammad Kazemi, Khorramdelazad Hossein, Zainodini Nahid, Shabani Ziba
Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Molecular-Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Clin Lab. 2014;60(1):93-7. doi: 10.7754/clin.lab.2013.121231.
Mycobacterium tuberculosis is a pulmonary pathogen responsible for tuberculosis. Tuberculosis (TB) is characterized histologically by granulomas at the site of disease activity. Primary pathologic feature of TB is formation of a granuloma, and chemokines are known to play an important role in the formation of granulomas during infection. Therefore, the aim of this study was to evaluate the serum levels of CCL11, CCL24, and CCL26 in the TB patients in comparison to healthy controls.
The population of this cross-sectional study included 300 patients suffering from TB and 100 healthy controls. Concentrations of CCL11, CCL24, and CCL26 were measured by enzyme linked immunosorbent assay (ELISA) technique. The results were analyzed using SPSS software package version 18. Differences were considered significant where p was less than 0.05.
The results showed significant elevated serum levels of CCL11, CCL24, and CCL26 in TB patients compared to controls.
According to the present results it can be concluded that CCL11, CCL24, and CCL26 (which are produced by Th2 cells and other cells which induce Th2 development) are increased in TB patients; hence, it seems that TB suppresses Th1 and the classic function of macrophages subsequently by inducing the chemokines' expression.
结核分枝杆菌是导致肺结核的病原体。肺结核在组织学上的特征是在疾病活动部位形成肉芽肿。肺结核的主要病理特征是肉芽肿的形成,并且已知趋化因子在感染期间肉芽肿的形成中起重要作用。因此,本研究的目的是评估肺结核患者与健康对照者血清中CCL11、CCL24和CCL26的水平。
这项横断面研究的人群包括300例肺结核患者和100名健康对照者。采用酶联免疫吸附测定(ELISA)技术测量CCL11、CCL24和CCL26的浓度。使用SPSS 18.0软件包分析结果。当p小于0.05时,差异被认为具有统计学意义。
结果显示,与对照组相比,肺结核患者血清中CCL11、CCL24和CCL26水平显著升高。
根据目前的结果可以得出结论,CCL11、CCL24和CCL26(由Th2细胞和其他诱导Th2发育的细胞产生)在肺结核患者中升高;因此,似乎肺结核通过诱导趋化因子的表达来抑制Th1和巨噬细胞的经典功能。