Figure 2. CXCR2 deficiency suppresses TPA-induced epidermal proliferation and neutrophil recruitment to inflamed skin.

(A and B) Shaved back skin of WT Balb/c mice received TPA once (A), or 3 times per week for 2 weeks (B), and was harvested 12–48 hours after the final TPA treatment. Relative expression of Cxcr2 and its ligands was determined by Q-RT-PCR; the mean of shaved, untreated skin (0 hours) is set to 1. *P < 0.05, **P < 0.01, ***P < 0.001 versus untreated, 1-way ANOVA with multiple comparison post-test. (C) Representative sections of anti-MPO–immunostained (brown) WT and Cxcr2^–/– Balb/c back skin 12 hours after a single TPA treatment. Sections were counterstained with hematoxylin and visualized by light microscopy. MPO⁺ cells in blood vessels are denoted by arrows. Original magnification, ×200. (D) Ki67⁺ epidermal cells in WT and Cxcr2^–/– (KO) Balb/c back skin 6, 12, and 24 hours either after a single TPA treatment (acute), or after the last of 6 TPA applications spanning 2 weeks (chronic). The mean of the maximal WT response in each data set is set to 100%. *P < 0.05, ***P < 0.001, 1-way ANOVA with multiple comparison post-test.