Neuronal expression of NOS-1 is required for host recovery from viral encephalitis

Takashi Komatsu; Derek D C Ireland; Nannan Chen; Carol Shoshkes Reiss

doi:10.1006/viro.1999.9734

Neuronal expression of NOS-1 is required for host recovery from viral encephalitis

Takashi Komatsu, Derek D C Ireland, Nannan Chen, Carol Shoshkes Reiss

Biology and Genomics

Research output: Contribution to journal › Article › peer-review

Abstract

The role of nitric oxide synthase (NOS) in host defense and clearance of vesicular stomatitis virus (VSV) from the central nervous system (CNS) was examined. NOS-1, NOS-2, and NOS-3 knockout mice were infected with VSV and were treated with either IL-12 or medium. IL-12 treatment resulted in substantially decreased VSV titers in wildtype and NOS-3 knockout mice, but had a marginal effect in the NOS-1 and NOS-2 knockout mice, NOS-1 expression in neurons was associated with survival from VSV infection. The data indicate that the enzyme activity is local, since NOS-2 expression in microglia and inflammatory macrophages and NOS-3 expression in astrocytes, endothelial cells, and ependymal cells did not compensate.

Original language	English (US)
Pages (from-to)	389-395
Number of pages	7
Journal	Virology
Volume	258
Issue number	2
DOIs	https://doi.org/10.1006/viro.1999.9734
State	Published - Jun 5 1999

Keywords

Acquired immunity
Innate immunity
Interleukin-12
Nitric oxide synthase
Viral infection

ASJC Scopus subject areas

Virology

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10.1006/viro.1999.9734

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@article{ea636483e2cb41e3873c13af56e5118e,

title = "Neuronal expression of NOS-1 is required for host recovery from viral encephalitis",

abstract = "The role of nitric oxide synthase (NOS) in host defense and clearance of vesicular stomatitis virus (VSV) from the central nervous system (CNS) was examined. NOS-1, NOS-2, and NOS-3 knockout mice were infected with VSV and were treated with either IL-12 or medium. IL-12 treatment resulted in substantially decreased VSV titers in wildtype and NOS-3 knockout mice, but had a marginal effect in the NOS-1 and NOS-2 knockout mice, NOS-1 expression in neurons was associated with survival from VSV infection. The data indicate that the enzyme activity is local, since NOS-2 expression in microglia and inflammatory macrophages and NOS-3 expression in astrocytes, endothelial cells, and ependymal cells did not compensate.",

keywords = "Acquired immunity, Innate immunity, Interleukin-12, Nitric oxide synthase, Viral infection",

author = "Takashi Komatsu and Ireland, {Derek D C} and Nannan Chen and Reiss, {Carol Shoshkes}",

note = "Funding Information: We gratefully acknowledge the gifts of breeding pairs of NOS-1 −/− and NOS-3 −/− mice from Paul Huang and Mark Fishman at MGH and of IL-12 from Genetics Institute. Mingee Kang, Steven A. Zimmer, and Sophie Stein contributed to many of the experiments performed in this study. This work was supported by Grant DC-03536 from the NIH to C.S.R.",

year = "1999",

month = jun,

day = "5",

doi = "10.1006/viro.1999.9734",

language = "English (US)",

volume = "258",

pages = "389--395",

journal = "Virology",

issn = "0042-6822",

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AU - Komatsu, Takashi

AU - Ireland, Derek D C

AU - Chen, Nannan

AU - Reiss, Carol Shoshkes

N1 - Funding Information: We gratefully acknowledge the gifts of breeding pairs of NOS-1 −/− and NOS-3 −/− mice from Paul Huang and Mark Fishman at MGH and of IL-12 from Genetics Institute. Mingee Kang, Steven A. Zimmer, and Sophie Stein contributed to many of the experiments performed in this study. This work was supported by Grant DC-03536 from the NIH to C.S.R.

PY - 1999/6/5

Y1 - 1999/6/5

N2 - The role of nitric oxide synthase (NOS) in host defense and clearance of vesicular stomatitis virus (VSV) from the central nervous system (CNS) was examined. NOS-1, NOS-2, and NOS-3 knockout mice were infected with VSV and were treated with either IL-12 or medium. IL-12 treatment resulted in substantially decreased VSV titers in wildtype and NOS-3 knockout mice, but had a marginal effect in the NOS-1 and NOS-2 knockout mice, NOS-1 expression in neurons was associated with survival from VSV infection. The data indicate that the enzyme activity is local, since NOS-2 expression in microglia and inflammatory macrophages and NOS-3 expression in astrocytes, endothelial cells, and ependymal cells did not compensate.

AB - The role of nitric oxide synthase (NOS) in host defense and clearance of vesicular stomatitis virus (VSV) from the central nervous system (CNS) was examined. NOS-1, NOS-2, and NOS-3 knockout mice were infected with VSV and were treated with either IL-12 or medium. IL-12 treatment resulted in substantially decreased VSV titers in wildtype and NOS-3 knockout mice, but had a marginal effect in the NOS-1 and NOS-2 knockout mice, NOS-1 expression in neurons was associated with survival from VSV infection. The data indicate that the enzyme activity is local, since NOS-2 expression in microglia and inflammatory macrophages and NOS-3 expression in astrocytes, endothelial cells, and ependymal cells did not compensate.

KW - Acquired immunity

KW - Innate immunity

KW - Interleukin-12

KW - Nitric oxide synthase

KW - Viral infection

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DO - 10.1006/viro.1999.9734

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AN - SCOPUS:0033526524

VL - 258

SP - 389

EP - 395

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -

Neuronal expression of NOS-1 is required for host recovery from viral encephalitis

Abstract

Keywords

ASJC Scopus subject areas

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