pubmed-article:10484466 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C0851887 | lld:lifeskim |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C0521026 | lld:lifeskim |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C2709248 | lld:lifeskim |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C1420002 | lld:lifeskim |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C0449297 | lld:lifeskim |
pubmed-article:10484466 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:10484466 | pubmed:issue | 3 Pt 1 | lld:pubmed |
pubmed-article:10484466 | pubmed:dateCreated | 1999-10-28 | lld:pubmed |
pubmed-article:10484466 | pubmed:abstractText | Surfactant protein A (SP-A) is a member of the collectin family of host defense molecules expressed primarily in the epithelial cells of the lung. To determine the role of SP-A in pulmonary adenoviral infection, SP-A-deficient (SP-A -/-) mice were intratracheally infected with a replication-deficient recombinant adenovirus, Av1Luc1. Lung inflammation was markedly increased in SP-A -/- compared with SP-A +/+ mice and was associated with increased hemorrhage and epithelial cell injury. Polymorphonuclear cells in bronchoalveolar lavage fluid (BALF) were increased in SP-A -/- mice after administration of adenovirus. Coadministration of adenovirus and purified human SP-A ameliorated adenoviral-induced lung inflammation in SP-A -/- mice. Concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, and IL-1beta were increased in BALF of SP-A -/- mice. Likewise, TNF-alpha, IL-6, macrophage inflammatory protein (MIP)-1alpha, monocyte chemotactic protein-1, and MIP-2 mRNAs were increased in lung homogenates from SP-A -/- mice 6 and 24 h after viral administration. Clearance of adenoviral DNA from the lung and uptake of fluorescent-labeled adenovirus by alveolar macrophages were decreased in SP-A -/- mice. SP-A enhances viral clearance and inhibits lung inflammation during pulmonary adenoviral infection, providing support for the importance of SP-A in antiviral host defense. | lld:pubmed |
pubmed-article:10484466 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10484466 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10484466 | pubmed:language | eng | lld:pubmed |
pubmed-article:10484466 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10484466 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10484466 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10484466 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10484466 | pubmed:month | Sep | lld:pubmed |
pubmed-article:10484466 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:10484466 | pubmed:author | pubmed-author:KorfhagenT... | lld:pubmed |
pubmed-article:10484466 | pubmed:author | pubmed-author:OtakeKK | lld:pubmed |
pubmed-article:10484466 | pubmed:author | pubmed-author:WhitsettJ AJA | lld:pubmed |
pubmed-article:10484466 | pubmed:author | pubmed-author:TrapnellB CBC | lld:pubmed |
pubmed-article:10484466 | pubmed:author | pubmed-author:HarrodK SKS | lld:pubmed |
pubmed-article:10484466 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10484466 | pubmed:volume | 277 | lld:pubmed |
pubmed-article:10484466 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10484466 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10484466 | pubmed:pagination | L580-8 | lld:pubmed |
pubmed-article:10484466 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:10484466 | pubmed:meshHeading | pubmed-meshheading:10484466... | lld:pubmed |
pubmed-article:10484466 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10484466 | pubmed:articleTitle | SP-A enhances viral clearance and inhibits inflammation after pulmonary adenoviral infection. | lld:pubmed |
pubmed-article:10484466 | pubmed:affiliation | Children's Hospital Medical Center, Division of Neonatology and Pulmonary Biology, Cincinnati, Ohio 45229, USA. | lld:pubmed |
pubmed-article:10484466 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10484466 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10484466 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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