巨噬细胞移动抑制因子
医学
基因
肺结核
免疫学
巨噬细胞
肺结核
遗传学
生物
病理
细胞因子
体外
作者
Shougang Kuai,Qinfang Ou,You De-hong,Zhongbo Shang,Jun Wang,Jun Liu,Xike Zhou,Pei Hao,Lihua Huang
标识
DOI:10.3109/23744235.2015.1107188
摘要
Objective: The role of the cytokine, macrophage migration inhibition factor (MIF) was assessed in tuberculosis. This case-control study investigated whether commonly occurring functional MIF polymorphisms are associated with active tuberculosis as well as with serum levels of MIF, IFN-γ and TNF-α. Methods: Two MIF promoter polymorphisms, a functional −794 CATT5–8 microsatellite repeat (rs5844572) and a −173G/C single-nucleotide polymorphism (rs755622), were analysed by PCR and PCR-RFLP, respectively, in 47 patients and 50 healthy subjects. The mRNA level of MIF was performed by real-time PCR (RT-PCR), and MIF, IFN-γ and TNF-α serum levels were determined by ELISA. Results: A significant increase of MIF mRNA expression and MIF protein level were found in patients compared to healthy controls. Meanwhile, the increase of IFN-γ and TNF-α serum levels were confirmed. According to the profile of genetic model, a significant association was found of genotypes carrying the −794 CATT7 or 8 and −173 C risk alleles with susceptibility to active tuberculosis and with a significant increase of MIF, IFN-γ and TNF-α. Conclusions: These data suggested a distinct genetic and immunopathogenic basis for tuberculosis at the MIF locus. Serum MIF, IFN-γ and TNF-α profiles distinguish tuberculosis from the more inflammatory phenotype and may play a role in pathogenesis and as biomarkers of active tuberculosis.
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