CIS-UROCANIC ACID STIMULATES HUMAN PERIPHERAL-BLOOD MONOCYTE PROSTAGLANDIN-E2 PRODUCTION AND SUPPRESSES INDIRECTLY TUMOR-NECROSIS-FACTOR-ALPHA LEVELS

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