成纤维细胞生长因子-7在巨噬细胞感染结核分枝杆菌中的免疫机制初步研究

Preliminary Research about the Immune Mechanism of Mycobacterium tuberculosis Infection Macrophages treated with Fibroblast Growth Factor-7

巨噬细胞分泌的纤维细胞生长因子-7(fibroblast growth factor-7,FGF-7)具有一定的细胞修复作用及抗炎症作用。通过PCR技术、Western-blot及ELISA实验研究分析FGF-7在巨噬细胞感染结核分枝杆菌(Mycobacterium tuberculosis,M.avium)后的分子免疫机制。研究发现fgf-7基因在结核病患者外周血单个核细胞中表达增强,并且U973巨噬细胞在感染M.avium后,其fgf-7基因与FGF-7蛋白亦表达增强,同时U973巨噬细胞上清中的细胞因子TNF-α与IFN-γ分泌量显著增加。实验结果表明巨噬细胞受M.avium感染后,M.avium可增强巨噬细胞fgf-7基因及其蛋白质的表达,并促进细胞因子TNF-α与IFN-γ的分泌;提示FGF-7可能与TNF-α、IFN-γ等共同引起炎症反应从而参与对M.avium的抑制或杀伤作用,并修复损伤的巨噬细胞。

Fibroblast growth factor-7 secreted from macrophages could repair damaged cells and has the anti- inflammatory effect. The molecular immune mechanisms of FGF-7 in Mycobacterium tuberculosis （M.avium） infection maerophages were analyzed by PCR technology, Western-blot and ELISA methods. The expression of fgf-7 gene was enhanced in peripheral blood mononuclear cells of TB patients and the fgf-7 gene and the FGF-7 protein were both increased in M.avium infection U973 macrophages.Meanwhile ,cytokines TNF-α and IFN-γ were also increased in the supernatants of U973 macrophages significantly. Results showed that M.avium could enhance the expression of fgf-7 gene and FGF-7 protein in macrophages and was able to promote macrophages to secrete more cytokines TNF-α, IFN-γ. It indicated that FGF-7 maybe cause the inflammation of maerophages associated with TNF-α, IFN-γ to kill M.avium and involve in repairing dam- aged macrophages.