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Eicosanoids in skin UV inflammation.

J Søndergaard, H Bisgaard, S Thorsen

    Photo-Dermatology
    |December 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    Eicosanoids, involved in UV inflammation, show varied release patterns. While prostaglandins E2 and F2 alpha

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    Area of Science:

    • Dermatology and Immunology
    • Biochemistry of Inflammation

    Background:

    • Eicosanoids are implicated as mediators in various types of ultraviolet (UV) induced inflammation.
    • Arachidonic acid metabolites, primarily cyclooxygenase (COX) products, are detected in human UV erythema exudates.

    Purpose of the Study:

    • To investigate the role of eicosanoids in the pathogenesis of UV-induced erythema.
    • To determine whether specific eicosanoids are causative agents or passive byproducts of UV-induced skin damage.

    Main Methods:

    • Analysis of eicosanoid concentrations and release patterns in UV-induced erythema.
    • Pharmacological inhibition studies using indomethacin to assess the role of prostaglandins.

    Main Results:

    • Eicosanoid concentration and release timing vary with UV type and erythema time course.

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  • Indomethacin partially inhibited UVB and UVC erythema, despite near-complete prostaglandin E2 and F2 alpha synthesis blockade.
  • Prostaglandin I2 (PGI2) is suggested as a more likely mediator due to its vascular proximity.

    • Conclusions:

    • The causative role of prostaglandins E and F in UV erythema remains uncertain.
    • Prostaglandin I2 is a potential mediator of UV erythema.
    • The lipoxygenase pathway's role in UV inflammation requires further exploration, with leukotrienes and hydroxy-fatty acids as potential contributors.