Complete reversal of acid-induced acute lung injury by blocking of platelet-neutrophil aggregation
J. Clin. Invest. Alexander Zarbock, et al. 116:3211 doi:10.1172/JCI29499 [
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Figure 4Neutrophil-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 TXB
2 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.
