Fig. 5.

CXCL5 contribution to UVB-induced pain-related hypersensitivity. (A and B) Animals received either a functional blocking CXCL5 antibody (Ab, 10 μg) or a control nonimmune IgG (10 μg) immediately after UVB irradiation, and again at 10 and 20 hours [shown by arrows in (A) and (B)]. Antibody neutralization of CXCL5 significantly attenuated the reduction in mechanical thresholds 30 hours after UVB (1000 mJ/cm²) (A). However, neutralization of this chemokine did not have an effect on thermal thresholds after UVB irradiation (B) (two-way repeated-measures ANOVA, n = 11). (C and D) At 8 hours after UVB irradiation, there was no change in infiltrating cell markers between treated and control animals. IBA1 mRNA expression was similar between CXCL5 antibody and the control IgG groups (C). Also, G-CSFR mRNA expression showed no change between groups (D). (E to H) At 30 hours after UVB irradiation, a time point at which the CXCL5-neutralizing antibody is effective in decreasing hypersensitivity behaviors, there was a significant reduction in IBA1 (E), G-CSFR (G), and CXCR2 mRNA expression (H) in animals treated with CXCL5-neutralizing antibody. No difference was found in CD3 mRNA expression (F) (*P < 0.05, t test; n = 4 to 6) (I to L) IBA1 staining in irradiated skin was reduced in animals treated with the CXCL5 antibody (K) versus vehicle (I). Low levels of CD3 staining were similarly detected in both groups (J and L) (scale bar, 200 μm). All data are presented as means ± SEM.