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Suppression of interleukin-6 increases enterovirus A71 lethality in mice
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نویسنده
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wang l.-c. ,yao h.-w. ,chang c.-f. ,wang s.-w. ,wang s.-m. ,chen s.-h.
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منبع
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journal of biomedical science - 2017 - دوره : 24 - شماره : 1
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چکیده
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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. © 2017 the author(s).
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کلیدواژه
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Enterovirus A71 and interleukin-6
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آدرس
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institute of basic medical sciences,national cheng kung university,tainan,701, Taiwan, center of infectious disease and signaling research,national cheng kung university,tainan,701, Taiwan, center of infectious disease and signaling research,national cheng kung university,tainan,701,taiwan,department of medical laboratory science and biotechnology,national cheng kung university,tainan,701, Taiwan, center of infectious disease and signaling research,national cheng kung university,tainan,701,taiwan,institute of molecular medicine,national cheng kung university,tainan,701, Taiwan, center of infectious disease and signaling research,national cheng kung university,tainan,701,taiwan,department of pediatrics,national cheng kung university,tainan,701, Taiwan, center of infectious disease and signaling research,national cheng kung university,tainan,701,taiwan,department of microbiology and immunology,college of medicine,national cheng kung university,tainan,701, Taiwan
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Authors
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