摘要
Background: Enterovirus A71 (EV-A71) infection can induce fatal encephalitis in young children. Clinical reports show that interleukin-6 (IL-6) levels in the serum and cerebrospinal fluid of infected patients with brainstem encephalitis are significantly elevated. We used a murine model to address the significance of endogenous IL-6 in EV-A71 infection. Results: EV-A71 infection transiently increased serum and brain IL-6 protein levels in mice. Most importantly, absence of IL-6 due to gene knockout or depletion of IL-6 using neutralizing monoclonal antibody enhanced the mortality and tissue viral load of infected mice. Absence of IL-6 increased the damage in the central nervous system and decreased the lymphocyte and virus-specific antibody responses of infected mice. Conclusions: Endogenous IL-6 functions to clear virus and protect the host from EV-A71 infection. Our study raises caution over the use of anti-IL-6 antibody or pentoxifylline to reduce IL-6 for patient treatment.
原文 | English |
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文章編號 | 94 |
期刊 | Journal of biomedical science |
卷 | 24 |
發行號 | 1 |
DOIs | |
出版狀態 | Published - 2017 12月 12 |
All Science Journal Classification (ASJC) codes
- 內分泌學、糖尿病和代謝
- 分子生物學
- 臨床生物化學
- 細胞生物學
- 生物化學(醫學)
- 藥學(醫學)