2002
DOI: 10.1152/ajpcell.00540.2001
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A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

Abstract: 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 hypothesized that priming of PMNs alters their reactivity such that a second priming agent causes PMN activation and endothelial cell damage. PMNs were primed or not with LPS and then treated with lyso-PCs, and oxidase activation and elastase release wer… Show more

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Cited by 134 publications
(206 citation statements)
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“…[21][22][23] These antibodies, lipids, or sCD40L activate neutrophils (PMNs), allowing for PMN-mediated endothelial damage, capillary leak, and acute lung injury (ALI). [6][7][8]13,24 We hypothesize that a prestorage filter that removes antibodies, leukocytes, and platelets and decreases lipid bioactivity would significantly decrease the presence of donor HLA antibodies and the accumulation of biologically active lipids and sCD40L and would abrogate TRALI in a 2-event animal model.…”
Section: Introductionmentioning
confidence: 99%
“…[21][22][23] These antibodies, lipids, or sCD40L activate neutrophils (PMNs), allowing for PMN-mediated endothelial damage, capillary leak, and acute lung injury (ALI). [6][7][8]13,24 We hypothesize that a prestorage filter that removes antibodies, leukocytes, and platelets and decreases lipid bioactivity would significantly decrease the presence of donor HLA antibodies and the accumulation of biologically active lipids and sCD40L and would abrogate TRALI in a 2-event animal model.…”
Section: Introductionmentioning
confidence: 99%
“…LPC (C16:0, 15 ”M) induces de-ramification of murine microglia, and nonselective cation current, and calciumactivated potassium current, with the subsequent hyperpolarization (Schilling et al, 2004) NEUTROPHILS LPC (1 ”M) alone slightly increases superoxide anion generation, and when co-treated with PMA, synergistically enhances PMA-induced superoxide anion generation (Englberger et al, 1987). Subsequent study showed that LPCs having fatty acids with more than 10 carbons enhance superoxide responses of stimulated human neutrophils (Ginsburg et al, 1989;Wyman et al, 2002). Lipids generated from stored blood were found to prime neutrophils, and identified to be LPCs (Silliman et al, 1994;Silliman et al, 1996).…”
Section: Neutrophilmentioning
confidence: 99%
“…One of characteristics of LPC actions is that LPC per se is a weak stimulator or even inactive, however, when LPC is combined with other stimulators, synergistic interactions often occurs (Englberger et al, 1987;Ginsburg et al, 1989;Asaoka et al, 1991;Asaoka et al, 1992;Sakai et al, 1994;Wyman et al, 2002). The most prominent example is seen in the priming of respiratory burst of neutrophils.…”
Section: Primingmentioning
confidence: 99%
“…28,29 These compounds effectively prime the PMN oxidative burst and can activate primed adherent PMNs both in vitro. [28][29][30][31] In addition an in vitro In response to an infection in the tissues, inflammatory signals (arrows) diffuse to the vasculature and activate the vascular endothelium causing release of chemokines (4-pointed stars), which attract PMNs to the endothelial surface. Attraction is followed by selectin-mediated PMN rolling and ÎČ 2 -integrin:ICAM-1 mediated firm adhesion of PMNs to endothelial cells (ECs).…”
Section: The Accumulation Of Pmn Priming Activity In Stored Bloodmentioning
confidence: 99%