Ultraviolet B radiation-induced production of interleukin 1alpha and interleukin 6 in a human squamous carcinoma cell line is wavelength-dependent and can be inhibited by pharmacological agents.
Ultraviolet (UV) B irradiation induces keratinocytes to produce among others the proinflammatory cytokines interleukin (IL) 1 and IL-6. The wavelength dependence of this UVB effect has not yet been assessed. We evaluated the potential of different UVB wavelength regions to release cytokines from the squamous carcinoma cell line SCL II and also assessed the effect of various putative inhibitors. Confluent monolayers of the cells were irradiated with 0.5-2.0 mJ/cm2 UVB at 280, 290, 300, 310 or 320 (each +/- 5) nm. In additional experiments dexamethasone (10-9-10-5 mol/L), ascorbic acid, d-alpha-tocopherol or indomethacin (each 10-7-10-4 mol/L) were added to the culture medium 24 h before, immediately after or combined before and after irradiation with 1 mJ/cm2 UVB at 280 +/- 5 nm. Supernatants of the cell cultures were recovered at 24 h after irradiation, and IL-1alpha or IL-6 were determined by an enzyme-linked immunosorbent assay (ELISA). IL-1alpha and IL-6 production were induced by UVB at 280, 290 and 300 nm, the production depended on the UV dose and decreased with increasing wavelengths. Irradiation at 310 or 320 nm did not induce cytokine production up to the maximum dose used. The production of IL-1 alpha/IL-6 was inhibited up to 80/89% (10-7-10-6 mol/L before and after irradiation) by dexamethasone in a concentration-dependent manner and with all conditions of incubation. Release of cytokines was also suppressed by indomethacin, d-alpha-tocopherol or ascorbic acid, but concentration dependence was not always evident. These results show that particularly shorter UVB radiation, which is expected to increase due to stratospheric ozone depletion, induces prominent production of proinflammatory cytokines, indicating major biological effects. Different pharmacological compounds can interfere with this effect and seem worth further evaluation with regard to their clinical effects.
Eberlein-König
B
B
Dermatologische Klinik und Poliklinik der Ludwig-Maximilians-Universität München, Frauenlobstr. 9-11, D-80337 Munich, Germany. Eberlein-Koenig@lrz.tu-muenchen.de
Jäger
C
C
Przybilla
B
B
D000368:Aged; D000369:Aged, 80 and over; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D002294:Carcinoma, Squamous Cell / Q000276:immunology* / Q000473:pathology; D002470:Cell Survival / Q000528:radiation effects; D004305:Dose-Response Relationship, Drug; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis*; D015850:Interleukin-6 / Q000096:biosynthesis*; D008297:Male; D009363:Neoplasm Proteins / Q000096:biosynthesis; D011829:Radiation Dosage; D013256:Steroids; D014407:Tumor Cells, Cultured; D014466:Ultraviolet Rays
D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D005938:Glucocorticoids; D007375:Interleukin-1; D015850:Interleukin-6; D009363:Neoplasm Proteins; D013256:Steroids