Table 2.

Recent Studies of Platelets in Murine Models of Acute Lung Injury

Model	Major Platelet Activities Examined and/or Variables Influenced by Platelets	Reference
LPS-induced ALI (aerosolized)	Lung neutrophil accumulation, increased alveolar–capillary permeability	66
LPS-induced ALI (intranasal)	Alveolar–capillary barrier function, inflammation-induced alveolar hemorrhage	77
LPS-induced ALI (intratracheal)	Intraalveolar platelet sequestration, platelet–neutrophil aggregate formation, increased alveolar–capillary permeability	43
LPS-induced ALI (intranasal)	Leukocyte recruitment to the lungs	36-38
LPS-induced ALI (aerosolized)	Neutrophil recruitment to lungs, increased alveolar–capillary permeability	170
LPS-induced ALI (intranasal)	Inflammation-induced alveolar hemorrhage	81
Klebsiella pneumoniae pneumonia, “pneumosepsis”	Bacterial burden in lungs, blood, systemic organs; inflammation-induced alveolar hemorrhage; leukocyte recruitment to lungs; NET formation; endothelial activation; cytokine concentrations; coagulation	76, 115
Streptococcus pneumoniae pneumonia	Bacterial burden in lungs, blood, spleen; cytokine concentrations; coagulation	102
Escherichia coli pneumonia	Platelet–leukocyte interaction, neutrophil recruitment to lungs, transcellular metabolism, platelet-endothelial signaling	39
H7N7 influenza A	Platelet accumulation in alveolar compartments, platelet–leukocyte interaction, platelet activation markers in BAL fluid, natural history of infection	104
H1N1 influenza A	Activation of platelets by influenza virus	106
CLP	Lung neutrophil accumulation, increased alveolar–capillary permeability	66
CLP	Lung neutrophil accumulation, lung edema, alveolar inflammation by histologic score	117
CLP	Lung neutrophil accumulation, lung edema, alveolar inflammation by histologic score	118
Acid-induced ALI	Increased alveolar–capillary permeability	32
Acid-induced ALI	Lung neutrophil accumulation, increased alveolar–capillary permeability	66
Acid-induced ALI	Lung endothelial cell activation, development of procoagulant lung endothelium	133
Acid-induced ALI	Platelet–neutrophil aggregation, alterations in lung barrier integrity induced by intravascular platelet–neutrophil interactions	132
Acid-induced ALI	Alveolar neutrophil accumulation, increased alveolar–capillary permeability, alveolar inflammation by histologic score	65
TRALI	Platelet sequestration in lungs, platelet–neutrophil interaction, increased alveolar–capillary permeability	32
TRALI	Platelet sequestration in lungs, NET formation, increased alveolar–capillary permeability	58
TRALI	Platelet–neutrophil interaction, increased alveolar–capillary permeability	43
TRALI	Neutrophil–platelet interaction, NET formation, pulmonary edema	33
TRALI	Platelets not required for increased alveolar–capillary permeability and decreased oxygenation but influenced alveolar hemorrhage in this study	142
VILI	Oxygenation, lung neutrophil accumulation, increased alveolar–capillary permeability	60

Definition of abbreviations: ALI = acute lung injury; CLP = cecal ligation and puncture; NET = neutrophil extracellular trap; TRALI = transfusion-related ALI; VILI = ventilator-induced lung injury.

The list of studies of platelets in experimental models of ALI in this table is not comprehensive, and other relevant investigations using animal models are mentioned in the text. Major variables and platelet activities examined in the studies are indicated, but many of the individual reports contain additional useful findings (e.g., effect on survival). In the listed studies, approaches to indicate contributions by platelets included induced or genetic thrombocytopenia, genetic alterations in platelet adhesion or signaling molecules, inhibition of platelet mediators, and/or administration of antiplatelet drugs or aspirin-triggered lipoxins. Earlier studies of platelets in experimental animal models are mentioned in the text and reviewed in References 12 and 14.