Abstract |
Intranasal infection of mice by Vesicular Stomatitis Virus (VSV) often leads to breakdown of the blood-brain barrier (BBB). The role of Interleukin 12 (IL-12) and nitric oxide synthase (NOS) was examined here. Wild-type (WT), NOS-1 knockout (KO), and NOS-3 KO mice were infected with VSV and treated with either IL-12 or medium. IL-12 treatment of uninfected hosts did not result in pathology. In contrast with WT and NOS-1 KO mice, where extensive gross and ultrastructural correlation of BBB breakdown were evident following infection, in NOS-3 KO mice, integrity of the BBB was observed. Thus NOS-3 activity in astrocytes, endothelial cells, or ependymal cells may play an essential role in regulating the BBB.
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Authors | T Komatsu, D D Ireland, N Chung, A Doré, M Yoder, C S Reiss |
Journal | Nitric oxide : biology and chemistry
(Nitric Oxide)
Vol. 3
Issue 4
Pg. 327-39
(Aug 1999)
ISSN: 1089-8603 [Print] United States |
PMID | 10444372
(Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Copyright | Copyright 1999 Academic Press. |
Chemical References |
- Coloring Agents
- Interleukin-12
- Nitric Oxide
- Evans Blue
- Nitric Oxide Synthase
- Nitric Oxide Synthase Type II
- Nitric Oxide Synthase Type III
- Nos2 protein, mouse
- Nos3 protein, mouse
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Topics |
- Animals
- Astrocytes
(enzymology)
- Blood-Brain Barrier
(physiology)
- Brain
(blood supply, ultrastructure)
- Coloring Agents
- Encephalitis, Viral
(enzymology, pathology, physiopathology)
- Endothelium, Vascular
(enzymology)
- Evans Blue
- Gap Junctions
(ultrastructure)
- Immunity, Innate
- Interleukin-12
(physiology)
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Nitric Oxide
(physiology)
- Nitric Oxide Synthase
(deficiency, genetics, physiology)
- Nitric Oxide Synthase Type II
- Nitric Oxide Synthase Type III
- Rhabdoviridae Infections
(enzymology, pathology, physiopathology)
- Specific Pathogen-Free Organisms
- Vesicular stomatitis Indiana virus
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