Figure 5.

Effects of Em on IMQ-induced psoriasis-like mouse model.(a) Representative images of psoriatic lesions on dorsal mouse skin in each treatment group after 7 days of treatment. (b) Evaluation of mouse clinical scores (desquamation, erythema, and thickness of the back skin) was assessed daily using a scale from 0 to 4 for 7 consecutive days for each group of 6 mice studied together. In additon, the cumulative total score PASI (scaling plus erythema plus thickness) is depicted as total PASI score over 7 days (low left panel) and as PASI score at day 7 for each treatment (low right panel), for a final total group of 18 mice per treatment, showing an increase of Em clinical efficiency by the presence of calcitriol in oil phase compared with emulsions without it. (c) Gene expression of cytokines was quantified from murine skin biopsies of the first 6 mice investigated for each group of treatment on day 7 using microfluidic qPCR. The results are shown as the gene expression of T-cell markers (CD3, CD4, CD8) and T-cell chemokines CCL17 and CCL20; the gene expression of psoriasis-associated proinflammatory cytokines (IL17A, IL17F, IL36α, and TNFα); as well as the one associated with epidermal cells, including K6a, β-DEF-2, LL37, S100a8, the anti-inflammatory IL38, or the dendritic cell–associated CD207 (Langerin). Symbols in b and in c indicate the mean value ± SEM of 18 mice and 6 mice per group, respectively, with ∗P < .05, ∗∗P < 0.01, and ∗∗∗P < 0.001 compared with the IMQ-applied-only mice. Statistical analysis was assessed using for experiment involving multiple groups, 1-way ANOVA followed by Turkey multiple comparison test, except for analysis of clinical scores, which used 2-way ANOVA followed by Dunnett’s multiple comparison test. B-DEF-2, β-defensin 2; Em, pickering emulsion; IMQ, imiquimod; K6a, keratin 6a.