Mouse strain differences in the chemokine response to acute lung infection with a murine gammaherpesvirus.

Mouse strain differences in the chemokine response to acute lung infection with a murine gammaherpesvirus.
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小鼠品系对鼠伽马疱疹病毒急性肺部感染的趋化因子反应存在差异。

DOI:
10.1089/088282404322875467
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发表时间:
2004
期刊:
Viral immunology.
影响因子:
--
通讯作者:
Rochford,Rosemary
Rochford,Rosemary
中科院分区:
--
文献类型:
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作者:
Weinberg,JasonB;Lutzke,MaryL;Alfinito,Rosiane;Rochford,Rosemary

文献摘要

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已经描述了在免疫应答和对许多病原体的易感性方面的许多基于小鼠品系的差异,但是不知道这些差异是否延伸到趋化因子应答, 肺部病毒感染。为了确定宿主趋化因子反应和对鼠γ疱疹病毒-68(MHV-68)感染易感性的小鼠品系差异,我们比较了诱导的趋化因子 BALB/c和C57 BL/6小鼠在感染后1-15天的肺中对MHV-68感染的应答。CC和CXC趋化因子在感染后的BALB/c和C57 BL/6中均被诱导,但趋化因子的水平在感染后的BALB/c和C57 BL/6中均被诱导。 对于所有测定的趋化因子,在BALB/c小鼠中的诱导显著更高。此外,干扰素-γ(IFN-γ)在肺中也被诱导至显著较高的水平 BALB/c感染小鼠与C57 BL/6小鼠相比。有趣的是,在复制的急性期,C57 BL/6小鼠的肺中的病毒基因表达较低。感染性病毒滴度也 在BALB/c肺中更大,尽管它们没有达到统计学显著性。相反,通过实时定量PCR测量的脾脏中的潜伏病毒载量, 小鼠品系,表明潜伏期的建立不受急性感染期间存在的病毒量的影响。该数据表明,感染的BALB/c小鼠肺中稳健的趋化因子应答和IFN-γ的表达与对感染的抗性增加无关。此外,观察到的趋化因子反应的显著差异将是需要考虑的重要因素 在未来的病毒发病机制研究中使用小鼠模型。
Numerous mouse strain-based differences in the immune response and in susceptibility to numerous pathogens have been described, but it is not known if these differences extend to chemokine responses to viral infection of the lungs. To define mouse strain-based differences in the host chemokine response and susceptibility to infection with murine gammaherpesvirus-68 (MHV-68), we compared the induced chemokine response to MHV-68 infection in the lungs of BALB/c and C57BL/6 mice at 1-15 days post-infection. CC and CXC chemokines were induced in both BALB/c and C57BL/6 following infection but the level of chemokine induction was significantly higher in the BALB/c mice for all chemokines measured. In addition, interferon-γ(IFN-γ) was also induced to a significantly higher level in the lungs of BALB/c infected mice compared to C57BL/6 mice. Interestingly, viral gene expression was lower in the lungs of C57BL/6 mice during the acute phase of replication. Titers of infectious virus were also greater in BALB/c lungs, although they did not achieve statistical significance. In contrast, latent viral load in the spleen, as measured by quantitative real-time PCR, did not significantly differ between mouse strains, suggesting that the establishment of latency is not affected by the amount of virus present during acute infection. This data suggests that robust chemokine response and expression of IFN-γin the lungs of infected BALB/c mice does not correlate with increased resistance to infection. In addition, the significant differences in chemokine responses observed will be important factors to consider in future studies of viral pathogenesis using mouse models.