摘要
目的探讨人巨细胞病毒(HCMV)感染对体外培养肺成纤维细胞(HEL)中明胶酶活性的影响。方法体外培养HEL细胞感染HCMV,分为低感染复数(MOI)组及高MOI组,每组重复6例。明胶酶谱法检测HEL细胞中MMP-2及MMP-9的明胶酶活性,用半定量RT-PCR检测各组HEL细胞中MMP-9及TIMP-1的转录水平。结果在低MOI组及高MOI组HEL细胞中MMP-9及MMP-2活性均增强(P<0.05),高MOI组MMP-9及MMP-2活性较低MOI组显著增加(P<0.05)。进一步检查MMP-9及TIMP-1的mRNA水平发现,正常对照组HEL细胞中MMP-9及TIMP-1的mRNA处于一个较低的水平,HCMV感染使HEL细胞中MMP-9及TIMP-1的mRNA水平均明显升高(P<0.05),低MOI组和高MOI组差异无统计学意义(P>0.05)。在低MOI组及高MOI组,HEL细胞MMP-9/TIMP-1的比值和正常对照组相比明显升高(P<0.05),表明MMP-9升高更为显著。高MOI组和低MOI组中MMP-9/TIMP-1的比值差异无统计学意义(P>0.05)。结论HCMV感染可以造成MMP-9和TIMP-1转录和MMP-9/TIMP-1的失衡,同时造成MMP-9及MMP-2明胶酶活性增强,导致肺泡结构的破坏和肺纤维化的发生,这在CMV肺炎的发病机制中起着重要的作用。
Objective -To-investigate the effect of HCMV infection on the activity of gelatinase in cultured human embryo lung fibroblast （HEL）. Methods The HEL cells were challenged with HCMV, and were grouped by multiplicity of infection（MOI） of HCMV, the uninfected cells serve as control group, and there were 6 cases in every group. The gelatinase activities of MMP-2 and MMP-9 were measured by gelatin zYmography and the transcriptional level MMP-9 and TIMP-1 were semiquantified by RT-PCR. Results The activities of MMP-2 and MMP-9 increased in HCMV infected cells in spit of the ratio of virus, but the intensive increase was found in high MOI group; The MMP-9 and TIMP-1 mRNA maintain a low level in uninfected HEL cells, they were up-regulated after HCMV challenge, and no significant difference was found between high MOI group and low MOI group; The ratio of MMP-9/TIMP-1 raised in both high MOI group and low MOI group and no difference was found between these two group. Conclusion HCMV infection can break balanceable transcription of MMP-9 and TIMP-1, cause the up-regulation of gelatinase activity, which may result in the destroy of alveolus structure and the occurrence of lung fibrosis. These pathogenic process play an important role in the mechanism of CMV pneumonia.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2005年第7期529-532,共4页
Chinese Journal of Microbiology and Immunology
