- 作者: Li-Chiu Wang, Hui-Wen Yao, Chuan-Fa Chang, Shainn-Wei Wang, Shih-Min Wang and Shun-Hua Chen
- 作者服務機構: 1. Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan 701, Republic of China 2. Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 701, Republic of China
- 中文摘要:
- 英文摘要:
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. - 中文關鍵字:
- 英文關鍵字: Enterovirus A71 and interleukin-6