Comparison of changes in endothelial adhesion molecule expression following UVB irradiation of skin and a human dermal microvascular cell line (HMEC‐1)

We have assessed the pattern of dermal endothelial adhesion molecule expression following broadband UVB irradiation in vivo and in vitro. Skin biopsies were taken from 4 human volunteers at baseline and at 4, 8 and 24 h post‐irradiation with 2.5 minimal erythema doses of UVB. Sections were stained immunohistochemically for E‐selectin, intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), CD31 and neutrophil elastase. The effect of direct UVB irradiation on E‐selectin, ICAM‐1 and VCAM‐1 was examined in a human dermal microvascular endothelial cell line, HMEC‐1. Cultured HMEC‐1 were irradiated with 2.5–40 mJ/cm 2 of UVB, and assessed for adhesion molecule expression by immunofluorescence microscopy and fluorescence‐activated cell sorter analysis. In vivo , E‐selectin was minimally expressed on EC at baseline and was induced by 4 h following irradiation, P <0.01. ICAM‐1 was moderately expressed at baseline and appeared mildly induced at 24 h, although this did not reach statistical significance. VCAM‐1 was weakly expressed in unirradiated skin while CD31 was moderately expressed, but neither was induced by UVB irradiation. A significant neutrophilic infiltrate appeared by 8 h and was maximal at 24 h, P <0.05. Neutrophil infiltration correlated with E‐selectin expression, r =0.96. In HMEC‐1, ICAM‐1 was upregulated at 24 h post‐irradiation, with an increase in mean channel fluorescence from 100% at baseline to 145 (SD12)%> at 24 h, P <0.05. No change was seen in expression of E‐selectin, VCAM‐1 or CD31. These studies support the involvement of endothelial adhesion molecules E‐selectin and ICAM‐1 in UVB‐induced inflammation. Whereas ICAM‐1 is upregulated by direct irradiation of endothelial cells, E‐selectin stimulation appears to be an indirect effect.