Abstract
Inflammatory erythema is primarily the gross manifestation of enhanced regional blood flow or hyperaemia. Hyperaemia to areas of injury is thought to modulate the delivery of circulating inflammatory cells to the responding site1,2 and in experimental models, it was shown synergistically to enhance the extravasation of plasma proteins and mediators3,4. It has recently been proposed that blood flow to inflammatory sites may be modulated by a novel vasoactive moiety, distinct from prostaglandins and plasminogen activator5,6, which is released by macrophages in response to antigenic or mitogenic stimulation. Intradermal (i.d.) injection of this hyperaemia-inducing activity (HIA) from activated macrophages elicited a sustained hyperaemia in the test rabbit7. We have now investigated this vasoactive mediator further. Using a sensitive assay for phospholipase A2 (PLA2)8, we have identified this enzyme in vasoactive conditioned medium of glycogen-induced peritoneal exudate cells (PEC) of rabbits. In the vasoactive conditioned medium, PLA2 and HIA cofractionated on gel filtration chromatography, and both the enzyme activity and biological activity were abrogated by treatment with the active site-directed histidine reagent p-bromophenacyl bromide (pBPB). Intradermal injection of PLA2 purified from snake venom induced a hyperaemia with kinetics resembling those of HIA. We propose that antigen-induced release of PLA2 by activated macrophages may mediate the hyperaemia associated with sites of chronic inflammation.
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Vadas, P., Wasi, S., Movat, H. et al. Extracellular phospholipase A2 mediates inflammatory hyperaemia. Nature 293, 583–585 (1981). https://doi.org/10.1038/293583a0
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DOI: https://doi.org/10.1038/293583a0
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