Advertisement

 

 

Suppression of interleukin-6 increases enterovirus A71 lethality in mice.

Suppression of interleukin-6 increases enterovirus A71 lethality in mice.
Author Information (click to view)

Wang LC, Yao HW, Chang CF, Wang SW, Wang SM, Chen SH,


Wang LC, Yao HW, Chang CF, Wang SW, Wang SM, Chen SH, (click to view)

Wang LC, Yao HW, Chang CF, Wang SW, Wang SM, Chen SH,

Advertisement
Share on FacebookTweet about this on TwitterShare on LinkedIn

Journal of biomedical science 2017 12 1224(1) 94 doi 10.1186/s12929-017-0401-5

Abstract
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.

Submit a Comment

Your email address will not be published. Required fields are marked *

four × five =

[ HIDE/SHOW ]