Literature DB >> 16617257

Animal models of transfusion-related acute lung injury.

Mark R Looney1, Michael A Matthay.   

Abstract

OBJECTIVE: To examine the existing animal models of transfusion-related acute lung injury (TRALI) for insight into disease pathogenesis. DATA SOURCE: The data were taken from published research and from our own experimental results.
RESULTS: Animal models have disproved the microaggregate theory of acute lung injury from blood transfusions. The two major hypotheses of TRALI, passively transfused neutrophil and human leukocyte antigen antibodies and biologically active lipids that accumulate in older, cellular blood products, have been replicated in animal models. The proposed two-hit model of TRALI is also supported by animal studies. A new in vivo mouse model of TRALI based on major histocompatibility complex (MHC) I antibodies has replicated several features of human TRALI, focusing prominently on the role of neutrophils.
CONCLUSIONS: Experimental animal models support both the antibody and lipid theories of TRALI. The essential role of neutrophils to producing lung injury is common to all existing models of TRALI. There is a lack of clinically relevant animal models that explain why transfusion of donor antibodies to cognate antigens in the recipient does not always lead to TRALI.

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Year:  2006        PMID: 16617257     DOI: 10.1097/01.CCM.0000214287.58444.2D

Source DB:  PubMed          Journal:  Crit Care Med        ISSN: 0090-3493            Impact factor:   7.598


  9 in total

1.  Extracellular DNA traps are associated with the pathogenesis of TRALI in humans and mice.

Authors:  Grace M Thomas; Carla Carbo; Brian R Curtis; Kimberly Martinod; Irina B Mazo; Daphne Schatzberg; Stephen M Cifuni; Tobias A Fuchs; Ulrich H von Andrian; John H Hartwig; Richard H Aster; Denisa D Wagner
Journal:  Blood       Date:  2012-05-17       Impact factor: 22.113

Review 2.  The mercurial nature of neutrophils: still an enigma in ARDS?

Authors:  Andrew E Williams; Rachel C Chambers
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2013-12-06       Impact factor: 5.464

3.  Transfusion-Related Acute Lung Injury (TRALI): Report of 2 Cases and a Review of The Literature.

Authors:  Bobby D Nossaman
Journal:  Ochsner J       Date:  2008

4.  Pretreatment with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitor SF1670 augments the efficacy of granulocyte transfusion in a clinically relevant mouse model.

Authors:  Yitang Li; Amit Prasad; Yonghui Jia; Saurabh Ghosh Roy; Fabien Loison; Subhanjan Mondal; Paulina Kocjan; Leslie E Silberstein; Sheng Ding; Hongbo R Luo
Journal:  Blood       Date:  2011-04-26       Impact factor: 22.113

Review 5.  Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques.

Authors:  Chrysi Keskinidou; Alice G Vassiliou; Ioanna Dimopoulou; Anastasia Kotanidou; Stylianos E Orfanos
Journal:  J Inflamm Res       Date:  2022-06-15

Review 6.  Blood Transfusion Reactions-A Comprehensive Review of the Literature including a Swiss Perspective.

Authors:  Theresa Ackfeld; Thomas Schmutz; Youcef Guechi; Christophe Le Terrier
Journal:  J Clin Med       Date:  2022-05-19       Impact factor: 4.964

7.  DUOX-Mediated Signaling Is Not Required for LPS-Induced Neutrophilic Response in the Airways.

Authors:  Sandra Chang; Angela Linderholm; Richart Harper
Journal:  PLoS One       Date:  2015-07-06       Impact factor: 3.240

8.  Resolvins Decrease Oxidative Stress Mediated Macrophage and Epithelial Cell Interaction through Decreased Cytokine Secretion.

Authors:  Ruan Cox; Oluwakemi Phillips; Jutaro Fukumoto; Itsuko Fukumoto; Prasanna Tamarapu Parthasarathy; Maria Mandry; Young Cho; Richard Lockey; Narasaiah Kolliputi
Journal:  PLoS One       Date:  2015-08-28       Impact factor: 3.240

Review 9.  Newly recognized causes of acute lung injury: transfusion of blood products, severe acute respiratory syndrome, and avian influenza.

Authors:  Mark R Looney
Journal:  Clin Chest Med       Date:  2006-12       Impact factor: 2.878

  9 in total

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