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 F1α was significantly elevated in blister fluids from five of six patients following antigen challenge In these subjects the levels of 6κ‐PGF1α 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 F1α, 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‐PGF1α 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.
|Original language||English (US)|
|Number of pages||6|
|Journal||British Journal of Dermatology|
|State||Published - Dec 1991|
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