[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 4th day was 1.1 and 1.5 times than that of the 7th and 14th day (P < 0.01). IP-10 showed similar expression between the 4th and 7th days (P > 0.05), which is 2.47 and 2.54 times compared to that of the 9th day (P < 0.01). And the expression of MCP-1 at the 14th day post-infection was 1.3, 1.2 and 1.0 times comparing to that of the 4th, 7th, 9th day post-infection, which showed statistical meaning. The expression of MCP-2 at the 4th was 1.4, 1.5 and 2.2 times comparing to that of the 7th, 9th, 14th 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.


CONCLUSIONS
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.
Shen
Yan
Y
Department of Immunology and Key Laboratory of Medical Molecular of Ministry of Education, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Xu
Wei
W
Shao
Xian-an
XA
Chen
Rui-zhen
RZ
Yang
Ying-zhen
YZ
Xiong
Si-dong
SD
D000818:Animals; D000914:Antibodies, Viral / Q000097:blood; D018925:Chemokines / Q000235:genetics*; D029822:Enterovirus B, Human / Q000276:immunology; D004769:Enterovirus Infections / Q000276:immunology*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009206:Myocardium / Q000378:metabolism*
D000914:Antibodies, Viral; D018925:Chemokines