Exposure to ultraviolet (UV) light impairs the function of inflammator
y cells. Urocanic acid (UCA) in an stratum corneum has been suggested
as a mediator in the immunosuppression of lymphoid cells detected afte
r irradiation with UVB (UV wavelengths 280-320 nm). In this study, we
examined the effects of the two UCA isomers, trans and cis UCA on huma
n polymorphonuclear leukocytes, neutrophils. It was found that treatme
nt of cells with either trans of cis UCA isomers inhibited the opsoniz
ed zymosan-induced respiratory burst activity, measured with luminol-e
nhanced chemiluminescence assay. Both isomers were also able to partia
lly block the up-regulation of complement receptors 1 (CR1: CD35) and
3 (CR3; CD11b/CD18) in N-formyl-methionyl-leucyl-phenylalanine (FMLP)-
stimulated neutrophils. These results indicate that the isomerization
of trans UCA to cis UCA is not essential for the action of UCA on neut
rophils. Neither of the UCA isomers were found to induce cyclic AMP (c
AMP) formation in 3-isobutyl-1-methylxanthine treated cells, suggestin
g that the activation of adenylate cyclase-cAMP system is not involved
in UCA provoked suppression of neutrophils. It is concluded that the
function of UCA may be protective, to suppress the activation of human
neutrophils in inflamed, sunburned epidermis.