Source:http://linkedlifedata.com/resource/pubmed/id/12626595
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2003-3-10
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| pubmed:abstractText |
Severe inflammation and mucus overproduction are partially responsible for respiratory syncytial virus (RSV)-induced disease in infants. Using a murine model, we characterized the virally induced chemokine receptors responsible for mediating the pathophysiological response to RSV infection, we found that CXCR2 mRNA was induced at 4 days after RSV infection. Immunohistochemical staining demonstrated that CXCR2 protein was expressed on alveolar macrophages. Immunoneutralization of CXCR2 resulted in decreased airway hyperreactivity relative to the RSV-infected controls. In addition, there was decreased mucus in the bronchoalveolar lavage fluid, decreased periodic-acid Schiff staining, and significantly less mucus-associated gob-5 mRNA and protein in anti-CXCR2-treated mice. The effects of anti-CXCR2 treatment were not a result of differences in viral clearance or neutrophil influx, as these parameters were comparable in both groups of animals. To confirm our immunoneutralization studies, we performed experiments in CXCR2(-/-) mice. Results in CXCR2(-/-) mice recapitulated results from our immunoneutralization studies. However, CXCR2(-/-) mice also showed a statistically significant decrease in muc5ac, relative to RSV-infected wild-type animals. Thus, CXCR2 may be a relevant target in the pathogenesis of RSV bronchiolitis, since it contributes to mucus production and airway hyperreactivity in our model of RSV infection.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
170
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3348-56
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:12626595-Animals,
pubmed-meshheading:12626595-Bronchial Hyperreactivity,
pubmed-meshheading:12626595-Bronchiolitis, Viral,
pubmed-meshheading:12626595-Disease Models, Animal,
pubmed-meshheading:12626595-Female,
pubmed-meshheading:12626595-Goblet Cells,
pubmed-meshheading:12626595-Humans,
pubmed-meshheading:12626595-Immune Sera,
pubmed-meshheading:12626595-Injections, Intraperitoneal,
pubmed-meshheading:12626595-Macrophages, Alveolar,
pubmed-meshheading:12626595-Metaplasia,
pubmed-meshheading:12626595-Mice,
pubmed-meshheading:12626595-Mice, Inbred BALB C,
pubmed-meshheading:12626595-Mice, Knockout,
pubmed-meshheading:12626595-Mucus,
pubmed-meshheading:12626595-Neutrophil Infiltration,
pubmed-meshheading:12626595-Receptors, Interleukin-8B,
pubmed-meshheading:12626595-Respiratory Syncytial Virus, Human,
pubmed-meshheading:12626595-Respiratory Syncytial Virus Infections
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| pubmed:year |
2003
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| pubmed:articleTitle |
CXCR2 regulates respiratory syncytial virus-induced airway hyperreactivity and mucus overproduction.
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| pubmed:affiliation |
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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