柯萨奇病毒B3感染对心肌趋化因子表达谱的调控作用

目的　研究柯萨奇病毒 (CV)B3感染对心肌组织 /细胞趋化因子 (ChKs)表达谱的调控作用。方法　以CVB3感染BALB/c小鼠和体外培养的BALB/c乳鼠心脏细胞 ,建立体内、外CVB3感染模型 ;RT PCR定性和实时定量分析不同CVB3感染时间点和不同CVB3载量下 1 1种ChKs的表达。结果　在体内 ,CVB3感染后心肌组织中MIP 2和IP 1 0诱导性表达 ,组成性表达的SDF 1、MCP 1、MCP 2、MCP 3、MCP 5、MDC、FKN和Ltn中MCP 1、MCP 2、MCP 3、MCP 5、MDC和Ltn上调表达 ,分别是未感染对照的 1 8、1 9、3 7、1 7、1 3和 1 2倍 ,均差异有显著性 (P均小于 0 0 1 ) ,SDF 1和FKN与未感染对照相比 ,差异均无显著意义 (P >0 0 5)。Eot在感染和未感染心肌组织均未检出表达。在不同的感染时间点ChKs的表达不同 ,MIP 2在感染第 4天的表达量分别是第 7天和第 1 4天的 1 1和 1 5倍 ,均差异有显著性 (P <0 0 1 ) ;IP 1 0的表达在第 4天和第 7天未表现显著性区别 (P >0 0 5) ,但分别是第 9天的 2 47和 2 54倍 (P <0 0 1 ) ;MCP 1第 1 4天的表达量分别是第4、7和 9天的 1 3、1 2和 1 0倍 ,相差均有显著性意义。MCP 2第 4天的表达量是第 7、9和 1 4天的1 4、1 5和 2 2倍 ,差异有显著意义 (P <0 0 1 ) ,且 1 4d表达量低于基础表

Infection of Coxsackievirus group B type 3 regulates the expression profile of chemokines in myocardial tissue/cells

Objective To investigate the role of Coxsackievirus group B type 3 (CVB3) infection on the expression profile of chemokines (ChKs) in myocardial tissue/cells Methods CVB3 was inoculated into male BALB/c intraperitoneally and primary neonatal myocardial cells of BALB/c to establish CVB3 infection models in vivo and in vitro, where the expression profile of ChKs was detected at different time points post infection as well as under different loading of CVB3 qualitatively and quantitatively by RT PCR Results The expression of MIP 2 and IP 10 was induced post infection, while SDF 1?MCP 1?MCP 2?MCP 3?MCP 5?MDC?FKN and Ltn were constitutively expressed in myocardial tissue The expression of MCP 1?MCP 2?MCP 3?MCP 5?MDC and Ltn increased 1 8?1 9?3 7?1 7?1 3 and 1 2 folds post infection higher than that of uninfected control ( P <0 01) There was not significant difference in the expression of SDF 1 and FKN between infected myocardial tissue and uninfected myocardial tissue ( P >0 05). The expression of Eot was not detected in infected and uninfected myocardial tissue Every chemokine had different expression at different infection time points For example, the expression of MIP 2 at the 4 th day was 1 1 and 1 5 times than that of the 7 th and 14 th day( P <0 01) IP 10 showed similar expression between the 4 th and 7 th days ( P >0 05), which is 2 47 and 2 54 times compared to that of the 9 th day ( P <0 01) And the expression of MCP 1 at the 14 th day post infection was 1 3?1 2 and 1 0 times comparing to that of the 4 th, 7 th , 9 th day post infection, which showed statistical meaning The expression of MCP 2 at the 4 th was 1 4?1 5 and 2 2 times comparing to that of the 7 th , 9 th , 14 th day, and moreover, the expression was lower than that of the basal expression The expression of MCP 1 and MCP 3 was up regulated significantly, which occurred at different time points post infection in vitro While the expression of MIP 2 and MCP 5 was down regulated in vitro The expression patterns of MCP 2, MCP 3, MCP 5 and MDC were consistent with CVB3 loading But that of the others (FKN , SDF 1,et al) were inconsistent with CVB3 loading There was a correlation between change patterns of MCP 3 and CVB3 loading post infection ( r =0 881, P <0 05) within 14 days after infection The varied expression trend of MCP 1 and MCP 3 was similar to the titer of anti CVB3 antibody ( r =0 913, P =0 031), while the expression of MCP 2, MCP 5 and MDC shows contrary change There was not a significant correlation between change patterns of other ChKs(IP 10,SDF 1,et al) and the titer of anti CVB3 antibody A positive correlation between anti CVB3 antibody and MCP 1( r =0 976, P <0 05)was showed Conclusion The expression level and kind of ChKs in vivo and in vitro was varied significantly in clusters after CVB3 infection The ChKs changed in clusters consisted of the expression profiles of ChKs There were complexity and unbalance in the change of the expression of ChKs in every expression profile It suggested that CVB3 infection could regulate the expression of ChKs in myocardial tissue/cells likely in different ways