Modulation of Acute Allergic Inflammation by Prostaglandins

Abstract

In vivo microscopy of the hamster cheek pouch microvasculature of sensitised animals was used for in vivo quantification of mediator release and the dynamic microcirculatory changes during immunologically induced acute mast cell-dependent inflammation. The evoked micro-vascular allergic reaction is probably IgE mediated and includes vasoconstriction followed by partially prostaglandin-dependent vasodilatation and immediate histamine-dependent plasma extravasation. The histamine-independent phase of plasma leakage is associated with leucocyte accumulation and is predominantly mediated by leukotrienes. Vasodilating prostaglandins [e.g. PGE2 (dinoprostone) and PGI2 (epoprostenol)] exert both pro- and anti-inflammatory actions, i.e. blood flow-dependent enhancement of inflammatory mediator action (oedema formation and leucocyte emigration) on one hand, and blood flow-independent suppression of mediator release on the other. In the hamster cheek pouch model of allergic inflammation, inhibition of mediator release by endogenous prostaglandins predominates. However, the final outcome of these opposite actions of vasodilating prostanoids is likely to vary with differences in experimental design. Accordingly, such a dual prostaglandin action may contribute to the understanding of the variable results of studies where NSAIDs or prostaglandins are used to modify different types of inflammation.