| Institution: | 1.Institute of Basic Medical Sciences,National Cheng Kung University,Tainan,Republic of China;2.Center of Infectious Disease and Signaling Research,National Cheng Kung University,Tainan,Republic of China;3.Department of Medical Laboratory Science and Biotechnology,National Cheng Kung University,Tainan,Republic of China;4.Institute of Molecular Medicine,National Cheng Kung University,Tainan,Republic of China;5.Department of Pediatrics,National Cheng Kung University,Tainan,Republic of China;6.Department of Microbiology and Immunology, College of Medicine,National Cheng Kung University,Tainan,Republic of China |
| Abstract: | BackgroundEnterovirus 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.ResultsEV-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.ConclusionsEndogenous 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. |
