Source:http://linkedlifedata.com/resource/pubmed/id/10190691
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1999-5-20
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pubmed:abstractText |
Mouse adenovirus-type 1 (MAV-1) has recently been shown to cause a fatal hemorrhagic encephalopathy in certain strains of mice whereas other strains are resistant. Morbidity is associated with a productive infection of cerebrovascular endothelial cells, resulting in necrosis of the vasculature, infarction, hemorrhage and death within 4 - 6 days. Previous studies were not able to define a role for the innate or acquired immune response. In the current study we have addressed the effect of MAV-1 on chemokine and chemokine receptor expression in the central nervous system (CNS) and spleen of susceptible (C57BL/6) and resistant (BALB/c) strains of mice. Intra-peritoneal infection with MAV-1 in C57BL/6 animals resulted in early and prominent induction of IP-10/crg-2 in the spleen and CNS. Increased expression of MCP-1, MIP-1alpha, MIP-1beta and RANTES was also noted in the CNS of MAV-1-infected C57BL/6 animals commencing around 72 h post-infection. In contrast, chemokine expression in BALB/c animals was more restricted with prominent upregulation only of MIP-2 in the CNS. In situ hybridization identified the vascular endothelium and CNS glia as the principal site of IP-10/crg-2 production in the C57BL/6 animals. The chemokine receptors CCR1-5 were upregulated in the CNS of both strains of mice. These data show that productive infection of the CNS with MAV-1 leads to the upregulation of a characteristic pattern of chemokines and their receptors, which may point to a role for these factors in disease pathogenesis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1355-0284
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
55-64
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10190691-Adenoviridae Infections,
pubmed-meshheading:10190691-Animals,
pubmed-meshheading:10190691-Brain Diseases,
pubmed-meshheading:10190691-Chemokine CXCL10,
pubmed-meshheading:10190691-Chemokines,
pubmed-meshheading:10190691-Chemokines, CXC,
pubmed-meshheading:10190691-Disease Susceptibility,
pubmed-meshheading:10190691-Female,
pubmed-meshheading:10190691-L Cells (Cell Line),
pubmed-meshheading:10190691-Mastadenovirus,
pubmed-meshheading:10190691-Mice,
pubmed-meshheading:10190691-Mice, Inbred BALB C,
pubmed-meshheading:10190691-Mice, Inbred C57BL,
pubmed-meshheading:10190691-RNA, Messenger,
pubmed-meshheading:10190691-Receptors, Chemokine,
pubmed-meshheading:10190691-Spleen,
pubmed-meshheading:10190691-Time Factors
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pubmed:year |
1999
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pubmed:articleTitle |
Differential chemokine induction by the mouse adenovirus type-1 in the central nervous system of susceptible and resistant strains of mice.
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pubmed:affiliation |
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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