No abstract

The present study assessed the molecular mechanism underlying ultraviolet (UV) B radiation-induced inhibition of the expression of the adhesion molecule ICAM-1 in human antigen-presenting cells (APC). UVB radiation-induced inhibition of ICAM-I expression in human peripheral blood monocytes was associated with the generation of cyclobutane pyrimidine dimers (CPD). CPD were reduced by 60% after treatment with liposomal packed photolyase, an enzyme which removes CPD after absorption of photoreactivating light. Although incomplete, reduction of CPD was associated with complete restoration of ICAM-1 expression at the mRNA and protein level. Neither reduction of CPD level nor restoration of ICAM-1 expression were observed, if monocytes were treated with empty liposomes, or if they were irradiated with photoreactivating light prior to application of photolyase. DNA damage might also induce soluble mediators capable of autocrine inhibition of ICAM-1 expression. UVB irradiation of monocytes did not induce IL-10 production, but resulted in release of prostaglandin (PG) E2. Treatment of unirradiated monocytes with PGE2 completely inhibited ICAM-1 expression, thus mimicking the UVB effect. Inhibition of monocytic PGE2 production by indomethacin, however, did not restore ICAM-1 expression. These results suggest that formation of CPD is necessary and sufficient for UVB radiation-induced inhibition of ICAM-1 expression. In contrast, PGE2 might serve a paracrine role in UVB radiation-induced immunosuppression.

No abstract

Immunocompromised patients are developing in an increasing frequency acyclovir-resistant herpes simplex infections. Different treatment options need to be evaluated considering the possible side effects in regard to the patients' immunocompromised status. A 73-year-old woman with B-cell lymphatic leukemia with a secondary antibody deficiency syndrome and anemia suffered for one year with perianal ulcerations caused by acyclovir-resistant herpes simplex infection Type II. Based on previous reports about successful treatment of acyclovir-resistant herpes simplex infections with foscarnet, cidofovir or vidarabine and considering the different side effects of these drugs as well as the underlying diseases of the patient, we treated her with foscarnet intravenously. After 3 months the ulcers showed a nearly complete remission.