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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2006-6-2
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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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16710475-10330041,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16710475-10439802,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16710475-10551607,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16710475-9525989
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
116
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1615-23
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16710475-Adoptive Transfer,
pubmed-meshheading:16710475-Animals,
pubmed-meshheading:16710475-Antibodies, Monoclonal,
pubmed-meshheading:16710475-Blood Transfusion,
pubmed-meshheading:16710475-Cell Membrane Permeability,
pubmed-meshheading:16710475-Disease Models, Animal,
pubmed-meshheading:16710475-Genes, MHC Class I,
pubmed-meshheading:16710475-Humans,
pubmed-meshheading:16710475-Lung,
pubmed-meshheading:16710475-Male,
pubmed-meshheading:16710475-Mice,
pubmed-meshheading:16710475-Mice, Inbred BALB C,
pubmed-meshheading:16710475-Mice, Knockout,
pubmed-meshheading:16710475-Neutrophils,
pubmed-meshheading:16710475-Organ Size,
pubmed-meshheading:16710475-Receptors, IgG,
pubmed-meshheading:16710475-Respiratory Distress Syndrome, Adult
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pubmed:year |
2006
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pubmed:articleTitle |
Neutrophils and their Fc gamma receptors are essential in a mouse model of transfusion-related acute lung injury.
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pubmed:affiliation |
Cardiovascular Research Institute, Department of Medicine, UCSF, San Francisco, California, USA. mark.looney@ucsf.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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