ABSTRACT
Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Subject(s)
Animals , Humans , Mice , Dermatitis, Contact , Dinitrofluorobenzene , Lymph Nodes , Prostaglandins E , Skin , Tissue DonorsABSTRACT
Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.