TY - JOUR
T1 - Ultraviolet B radiation-induced production of interleukin 1α and interleukin 6 in a human squamous carcinoma cell line is wavelength-dependent and can be inhibited by pharmacological agents
AU - Eberlein-König, B.
AU - Jäger, C.
AU - Przybilla, B.
PY - 1998
Y1 - 1998
N2 - 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 (10-910-5 mol/L), ascorbic acid, d-α-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-1α or IL-6 were determined by an enzyme-linked immunosorbent assay (ELISA). IL-1α 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 α/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-α-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.
AB - 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 (10-910-5 mol/L), ascorbic acid, d-α-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-1α or IL-6 were determined by an enzyme-linked immunosorbent assay (ELISA). IL-1α 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 α/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-α-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.
UR - http://www.scopus.com/inward/record.url?scp=0031684665&partnerID=8YFLogxK
U2 - 10.1046/j.1365-2133.1998.02404.x
DO - 10.1046/j.1365-2133.1998.02404.x
M3 - Article
C2 - 9767285
AN - SCOPUS:0031684665
SN - 0007-0963
VL - 139
SP - 415
EP - 421
JO - British Journal of Dermatology
JF - British Journal of Dermatology
IS - 3
ER -
