JCI - Complete reversal of acid-induced acute lung injury by blocking of platelet-neutrophil aggregation

Complete reversal of acid-induced acute lung injury by blocking of platelet-neutrophil aggregation

Alexander Zarbock, Kai Singbartl, Klaus Ley

Published in Volume 116, Issue 12

J Clin Invest. 2006; 116(12):3211–3219 doi:10.1172/JCI29499

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Figure 4

Neutrophil-platelet adhesion to untreated HPMECs requires endothelial cell TPs.

(A) Platelet-neutrophil interactions significantly induced PMN adhesion (n = 3 per group). (B) Increased adhesion was partially mediated by endothelial cell TPs. Baseline PMN adhesion is indicated by dotted line. (C) ICAM-1 mRNA in endothelial cells was increased by exposure to activated PMNs or the combination of PMNs and platelets when at least 1 of the cell types was activated (n = 3 per group). (D) The incubation of human platelets with neutrophils induced a 2.5-fold increase in TXB₂ measured in the supernatant, which was further enhanced to 5.5-fold when either PMNs or platelets were activated by TNF-α or thrombin. n = 3 per group. ^&P < 0.05 versus PMNs; ^ΧP < 0.05 versus both and activated PMNs; *P < 0.05 versus vehicle; ^#P < 0.05 versus control; ^†P < 0.05 versus platelets. Act., activated; plt., platelet.