基质金属蛋白酶表达与嗜神经性小鼠肝炎病毒感染后的毒力相关。
Matrix metalloproteinase expression correlates with virulence following neurotropic mouse hepatitis virus infection.
作者信息
Zhou Jiehao, Stohlman Stephen A, Atkinson Roscoe, Hinton David R, Marten Norman W
机构信息
Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.
出版信息
J Virol. 2002 Aug;76(15):7374-84. doi: 10.1128/jvi.76.15.7374-7384.2002.
Abstract
The relationship(s) between viral virulence and matrix metalloproteinase (MMP) expression in the central nervous system (CNS) of mice undergoing lethal and sublethal infections with neurotropic mouse hepatitis virus was investigated. Lethal infection induced increased levels of MMP-3 and MMP-12 mRNAs as well as that of tissue inhibitor of matrix metalloproteinases 1 (TIMP-1) compared to sublethal infection. Increased induction of MMP, TIMP, and chemokine expression correlated with increased virus replication but not with inflammatory cell infiltration. Infection of immunosuppressed mice suggested that expression of most MMP, TIMP, and chemokine mRNA was induced primarily in CNS-resident cells. By contrast, MMP-9 protein activity was associated with the infiltration of neutrophils into the CNS. These data indicate an association between the magnitude of inflammatory gene expression within the CNS and viral virulence.
摘要
研究了嗜神经性小鼠肝炎病毒致死性和亚致死性感染小鼠中枢神经系统（CNS）中病毒毒力与基质金属蛋白酶（MMP）表达之间的关系。与亚致死性感染相比，致死性感染诱导MMP-3和MMP-12 mRNA以及基质金属蛋白酶组织抑制剂1（TIMP-1）水平升高。MMP、TIMP和趋化因子表达的诱导增加与病毒复制增加相关，但与炎性细胞浸润无关。免疫抑制小鼠的感染表明，大多数MMP、TIMP和趋化因子mRNA的表达主要在中枢神经系统驻留细胞中诱导。相比之下，MMP-9蛋白活性与中性粒细胞向中枢神经系统的浸润有关。这些数据表明中枢神经系统内炎性基因表达的程度与病毒毒力之间存在关联。
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