Cutting edge: Oseltamivir decreases T cell GM1 expression and inhibits clearance of respiratory syncytial virus: Potential role of endogenous sialidase in antiviral immunity

被引:36
作者
Moore, Martin L.
Chi, Michael H.
Zhou, Weisong
Goleniewska, Kasia
O'Neal, Jamye F.
Higginbotham, James N.
Peebles, R. Stokes, Jr.
机构
[1] Vanderbilt Univ, Med Ctr, Sch Med, Dept Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37232 USA
关键词
D O I
10.4049/jimmunol.178.5.2651
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The sialoglycosphingolipid GM1 is important for lipid rafts and immune cell-signaling. T cell activation in vitro increases GM1 expression and increases endogenous sialidase activity. GM1 expression has been hypothesized to be regulated by endogenous sialidase. We tested this hypothesis in vivo using a mouse model of respiratory syncytial virus (RSV) infection. RSV infection increased endogenous sialidase activity in lung mononuclear cells. RSV infection increased lung CD8(+) T cell surface GM1 expression. Activated CD8(+) T cells in the hings of RSV-infected mice were GM1(high). Treatment of RSV-infected mice with the sialidase/neuraminidase inhibitor oseltamivir decreased T cell surface GM1 levels. Oseltamivir treatment decreased RSV-induced weight loss and inhibited,RSV clearance. Our data indicate a novel role for an endogenous sialidase in regulating T cell GM1 expression and antiviralimmunity. Also, oseltamivir, an important anti influenza drug, inhibits the clearance of a respiratory virus that lacks a neuranzinidase gene, RSV.
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页码:2651 / 2654
页数:4
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