| pubmed-article:16710475 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16710475 | lifeskim:mentions | umls-concept:C1522424 | lld:lifeskim |
| pubmed-article:16710475 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:16710475 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:16710475 | lifeskim:mentions | umls-concept:C0123263 | lld:lifeskim |
| pubmed-article:16710475 | lifeskim:mentions | umls-concept:C1719482 | lld:lifeskim |
| pubmed-article:16710475 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:16710475 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:16710475 | pubmed:dateCreated | 2006-6-2 | lld:pubmed |
| pubmed-article:16710475 | pubmed:abstractText | Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion-related mortality. To explore the pathogenesis of TRALI, we developed an in vivo mouse model based on the passive transfusion of an MHC class I (MHC I) mAb (H2Kd) to mice with the cognate antigen. Transfusion of the MHC I mAb to BALB/c mice produced acute lung injury with increased excess lung water, increased lung vascular and lung epithelial permeability to protein, and decreased alveolar fluid clearance. There was 50% mortality at a 2-hour time point after Ab administration. Pulmonary histology and immunohistochemistry revealed prominent neutrophil sequestration in the lung microvasculature that occurred concomitantly with acute peripheral blood neutropenia, all within 2 hours of administration of the mAb. Depletion of neutrophils by injection of anti-granulocyte mAb Gr-1 protected mice from lung injury following MHC I mAb challenge. FcRgamma-/- mice were resistant to MHC I mAb-induced lung injury, while adoptive transfer of wild-type neutrophils into the FcRgamma-/- animals restored lung injury following MHC I mAb challenge. In conclusion, in a clinically relevant in vivo mouse model of TRALI using an MHC I mAb, the mechanism of lung injury was dependent on neutrophils and their Fc gamma receptors. | lld:pubmed |
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| pubmed-article:16710475 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16710475 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16710475 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16710475 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16710475 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16710475 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:16710475 | pubmed:author | pubmed-author:MatthayMichae... | lld:pubmed |
| pubmed-article:16710475 | pubmed:author | pubmed-author:LowellCliffor... | lld:pubmed |
| pubmed-article:16710475 | pubmed:author | pubmed-author:SuXiaoX | lld:pubmed |
| pubmed-article:16710475 | pubmed:author | pubmed-author:LooneyMark... | lld:pubmed |
| pubmed-article:16710475 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:16710475 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16710475 | pubmed:volume | 116 | lld:pubmed |
| pubmed-article:16710475 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16710475 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16710475 | pubmed:pagination | 1615-23 | lld:pubmed |
| pubmed-article:16710475 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16710475 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16710475 | pubmed:articleTitle | Neutrophils and their Fc gamma receptors are essential in a mouse model of transfusion-related acute lung injury. | lld:pubmed |
| pubmed-article:16710475 | pubmed:affiliation | Cardiovascular Research Institute, Department of Medicine, UCSF, San Francisco, California, USA. mark.looney@ucsf.edu | lld:pubmed |
| pubmed-article:16710475 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16710475 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16710475 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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