Role of neutrophils in the deposition of platelets during acute inflammation.
Platelets can release a variety of inflammatory mediators. These formed elements have been shown to accumulate early in acute inflammation, often prior to fibrin and thrombus formation. Polymorphonuclear leukocyte (PMNL) infiltration is also an early event and is linked to protein exudation and hyperemia. The relationship between PMNL and platelet accumulation was studied. Inflammation was induced in rabbits by intradermal injection of stimuli, and 51Cr-labeled leukocytes and 111In-labeled platelets were used to quantitate the rates of leukocyte and platelet accumulation in the dermal reactions. A temporal association between the rates of leukocyte infiltration (greater than 95% PMNL) and of platelet deposition at skin sites was observed when killed Escherichia coli, E. coli-derived chemotactic factors, zymosan-activated plasma, f-met-leu-phe, or endotoxin were injected intradermally. A linear correlation (r = 0.96; p less than 0.001) between these parameters was observed. 59Fe-labeled red cells did not accumulate in these lesions. Platelet deposition in response to inflammatory stimuli did not occur in PMNL-depleted (nitrogen mustard treatment) but platelet-sufficient rabbits, in spite of normal platelet deposition in thrombin-injected sites. Platelet responses to inflammatory stimuli were normal when neutropenia, after nitrogen mustard treatment, was prevented. In contrast, in situ PMNL reconstitution of the skin sites in neutropenic rabbits did not cause local platelet accumulation. Intravenous infusion of the synthetic chemotactic factor, f-met-leu-phe, induced transient neutropenia and thrombocytopenia (30% of control) with platelet sequestration primarily in the lung. This is also the known site of PMNL sequestration during f-met-leu-phe infusion. It is concluded that platelets selectively deposit in acutely inflamed tissues primarily during PMNL margination in, and emigration across, the microvasculature. Platelets and PMNLs likely coassociate on the vessel wall, and this interaction may influence the course of inflammation.
D000208:Acute Disease; D000818:Animals; D002630:Chemotactic Factors / Q000502:physiology; D002634:Chemotaxis, Leukocyte; D004731:Endotoxins / Q000633:toxicity; D004926:Escherichia coli; D004927:Escherichia coli Infections / Q000097:blood / Q000503:physiopathology; D005260:Female; D007249:Inflammation / Q000097:blood* / Q000503:physiopathology; D008297:Male; D009504:Neutrophils / Q000502:physiology*; D010974:Platelet Aggregation; D011817:Rabbits
D002630:Chemotactic Factors; D004731:Endotoxins