cis-Urocanic acid stimulates human peripheral blood monocyte prostaglandin E2 production and suppresses indirectly tumor necrosis factor-α levels

P. H. Hart, C. A. Jones, K. L. Jones, C. J. Watson, I. Santucci, L. K. Spencer, J. J. Finlay-Jones

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Photoisomerization of trans-urocanic acid (UCA) in the stratum corneum has been implicated in the immunosuppression detected after irradiation with UVB (UV wavelength of 280-320 nm). In this study, cis-urocanic acid suppressed human monocyte production of TNF-α by a PGE2-dependent mechanism. This contrasted with the mechanism involving histamine type 2 receptors by which the UCA structural analogue, histamine, suppressed monocyte TNF-α production. Histamine type 1 receptor antagonists were without effect on both the cis-UCA- and histamine-induced suppression of monocyte TNF-α levels. As indomethacin can reverse UVB-immunosuppression in murine models, we may have identified one of the cellular mechanisms responsible for reduced delayed- type hypersensitivity responses. Decreased TNF-α levels, by restricting further cytokine recruitment, may also limit the development of the inflammatory components of hypersensitivity responses.

Original languageEnglish
Pages (from-to)4514-4523
Number of pages10
JournalJournal of Immunology
Volume150
Issue number10
Publication statusPublished - 1 Jan 1993
Externally publishedYes

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