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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
This article Copyright © 2006, The American Society for Clinical Investigation
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Figure 3
Platelet P-selectin plays key role in the development of ALI.

(A–C) Injecting P-selectin Abs 15 minutes after the induction of ALI (n = 4–5 mice per group) improved gas exchange (A) and reduced interstitial (data not shown) and BAL fluid (B) PMNs as well as permeability (C). (D–G) To determine whether hematopoietic (platelet) or nonhematopoietic (endothelial) P-selectin is responsible for neutrophil recruitment in ALI, BM chimeras (WT into WT; WT into Selp–/–; Selp–/– into WT; Selp–/– into Selp–/–) were tested (n = 4–5 mice per group). Mice lacking platelet P-selectin showed improved gas exchange (D), reduced PMN accumulation in the intravascular (E), interstitial (data not shown), and alveolar compartments (F), and diminished permeability (G) compared with mice expressing hematopoietic P-selectin. #P < 0.05; ΧP < 0.05 versus platelet Selp–/–.

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