Profile of prostanoid release following antigen challenge in vivo in the skin of man

Summary We have previously characterized the kinetics of prostaglandin D₂ (PGD₂) production at cutaneous sites of allergic inflammation employing a blister‐chamber model. In this study, a more complete profile of prostaglandins released in vivo was obtained, PGD₂ release, as measured by radioimmunoassay and by combined gas chromatographymass spectrometry, was evident within 1h after antigen challenge with maximal levels occurring 3–4 h post‐challenge. The 11‐ketoreductase metabolite of PGD₂, 9α, 11β‐prostaglandin F₂ was present in blister fluid from three of six patients at the time of maximal levels of PGD₂. The stable non‐enzymatic hydrolysis product of prostacyclin, 6‐keto‐prostaglandin F_1α was significantly elevated in blister fluids from five of six patients following antigen challenge In these subjects the levels of 6κ‐PGF_1α were highest in samples obtained 1 and 2 h after antigen challenge and remained significantly elevated until 5 h post‐challenge. Levels of prostaglandin E₂, prostaglandin F_1α, and thromboxane B₂ did not vary significantly. These studies suggest that following antigen challenge two fatty‐acid cyclo‐oxygenase products of arachidonic acid are released, PGD₂ and prostacyclin. The 11‐ketoreductase metabolism of PGD₂ to 9α, 11β‐PGF2 could represent a mechanism by which the biological effects of PGD₂ are prolonged in cutaneous tissue. The presence of 6κ‐PGF_1α in the blister fluid suggests that significant prostacyclin release occures as the results of antigen challenge and could represent a mechanism by which the prologed microvascular response in cutaneous tissue may occur.