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Cis ‐UROCANIC ACID SYNERGIZES WITH HISTAMINE FOR INCREASED PGE 2 PRODUCTION BY HUMAN KERATINOCYTES: LINK TO INDOMETHACIN‐INHIBITABLE UVB‐INDUCED IMMUNOSUPPRESSION
Author(s) -
Jaksic Aleksandra,
FinlayJones John J.,
Watson Christopher J.,
Spencer Lyn K.,
Santucci Irma,
Hart Prue H.
Publication year - 1995
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1995.tb03976.x
Subject(s) - urocanic acid , histamine , sensitization , chemistry , prostaglandin e2 , in vitro , prostaglandin e , keratinocyte , foreskin , prostaglandin , immune system , immunology , microbiology and biotechnology , pharmacology , biology , endocrinology , biochemistry , cell culture , enzyme , histidine , genetics
— There is considerable evidence that suppression of the immune system by UVB (280–320 nm UV) irradiation is initiated by UVB‐dependent isomerization of a specific skin photoreceptor, urocanic acid (UCA), from the trans to the cis form. Previous studies have confirmed that cis ‐UCA administration to mice 3–5 days prior to hapten sensitization at a distant site, suppresses the contact hypersensitivity (CHS) response upon challenge. This study demonstrates in mice that cis ‐UCA, like UVB, suppresses CHS to trinitrochlorobenzene by a mechanism partly dependent on prostanoid production. In vitro experimentation showed that human keratinocytes, isolated from neonatal foreskin, increased prostaglandin E 2 (PGE 2 ) production in response to histamine but not UCA alone. However, cis ‐UCA synergized with histamine for increased PGE 2 production by keratinocytes. cis ‐urocanic acid also increased the sensitivity of keratinocytes for PGE 2 production in response to histamine. Prostaglandin E 2 from keratinocytes exposed to cis ‐UCA and histamine may contribute directly, or indirectly, to the regulation of CHS responses by UVB irradiation.