在CXCL10缺陷小鼠中，抗肿瘤坏死因子α抗体可阻断单纯疱疹病毒2型引起的生殖器感染后的死亡。
Herpes simplex virus type 2-induced mortality following genital infection is blocked by anti-tumor necrosis factor alpha antibody in CXCL10-deficient mice.
作者信息
Thapa Manoj, Carr Daniel J J
机构信息
Department of Ophthalmology, DMEI #415, University of Oklahoma Health Sciences Center, 608 Stanton L Young Blvd., Oklahoma City, OK 73104, USA.
出版信息
J Virol. 2008 Oct;82(20):10295-301. doi: 10.1128/JVI.00931-08. Epub 2008 Aug 6.
Abstract
The role of tumor necrosis factor alpha (TNF-alpha) was evaluated for CXCL10-deficient (CXCL10(-/-)) mice which succumbed to genital herpes simplex virus type 2 (HSV-2) infection and possessed elevated levels of virus and TNF-alpha but not other cytokines in the central nervous system (CNS) and vaginal tissue within the first 7 days following virus exposure. Anti-TNF-alpha but not control antibody treatment offsets the elevated mortality rate of CXCL10(-/-) mice, despite increased CNS viral titers. In addition, TNF-alpha neutralization suppressed recruitment of leukocyte subpopulations into the CNS, which is associated with reduced CCL2 and CXCL9 expression. Collectively, the results implicate TNF-alpha as the principal mediator of mortality in response to genital HSV-2 infection.
摘要
对趋化因子CXCL10缺陷型（CXCL10(-/-)）小鼠进行了研究，以评估肿瘤坏死因子α（TNF-α）的作用。这些小鼠在感染2型单纯疱疹病毒（HSV-2）后死亡，且在病毒暴露后的头7天内，其在中枢神经系统（CNS）和阴道组织中的病毒水平和TNF-α水平升高，但其他细胞因子水平未升高。尽管中枢神经系统病毒滴度增加，但抗TNF-α而非对照抗体治疗可降低CXCL10(-/-)小鼠的死亡率。此外，TNF-α中和作用抑制了白细胞亚群向中枢神经系统的募集，这与CCL2和CXCL9表达降低有关。总体而言，这些结果表明TNF-α是生殖器HSV-2感染致死的主要介质。
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