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Articles in PresS, published online ahead of print July 24, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00540.2001
Submitted on November 13, 2001
Accepted on July 19, 2002
1 Research, Bonfils Blood Center, Denver, CO, USA; Pediatrics and Surgery, University of Colorado School of Medicine, Denver, CO, USA
2 Leukocyte Biology, Baylor College of Medcine, Houston, TX, USA
3 Pediatrics and Surgery, University of Colorado School of Medicine, Denver, CO, USA
4 Research, Bonfils Blood Center, Denver, CO, USA; Pediatrics and Surgery, University of Colorado School of Medicine, Denver, CO, USA; Leukocyte Biology, Baylor College of Medcine, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: christopher.silliman{at}uchsc.edu.
Lysophosphatidylcholines (lyso-PCs), generated during blood storage, are etiologic in a two-insult, sepsis-based, model of transfusion related acute lung injury (TRALI). Individually endotoxin (LPS) and lyso-PCs prime but do not activate neutrophils (PMNs). We hypothesize that priming of PMNs alters their reactivity, such that a second priming agent causes PMN activation and endothelial damage. PMNs were primed ± LPS, treated with lyso-PCs and oxidase activation and elastase release were measured. For co-culture experiments, activation of human pulmonary microvascular endothelial cells (HMVECs) was assessed by ICAM-1 expression and chemokine release. HMVECs were stimulated ± LPS, PMNs were added, incubated with lyso-PCs, and the number of viable HMVECs was counted. Lyso-PCs activated LPS-primed PMNs. HMVEC activation resulted in increased ICAM-1 and release of ENA-78, GRO
, and IL-8. PMN-mediated HMVEC damage was dependent upon LPS activation of HMVECs, chemokine release, PMN adhesion, and lyso-PC activation of the oxidase. In conclusion, sequential exposure of PMNs to priming agents activates the microbicidal arsenal, and PMN-mediated HMVEC damage was the result of two insults: HMVEC activation and PMN oxidase assembly.
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