Figure 2. Absence of Th2 signaling enhances antimicrobial defense against S. aureus.
(A–C) Expression of Camp (A), Defb14 (B), and Defb4 (C) in the skin of WT or Il4ra−/− mice after treatment with MC903 and S. aureus (SA) application. Each dot represents the average of duplicate technical replicates from an individual animal. Data represent mean ± SEM of 5 independent mice. p value (**p < 0.01) was calculated by two-tailed Mann-Whitney U test.n.
(D) Immunofluorescence for CRAMP (a gene product of Camp) in the skin of WT or Il4ra−/− mice after treatment with MC903 and S. aureus application. Scale bar: 100 μm. Image is representative of similar results from indicated 5 biological replicates.
(E) Survival of S. aureus on the skin of WT or Il4ra−/− mice pretreated with MC903 or vehicle for 48 h (WT: n = 5; Il4ra−/−: n = 10). Each dot represents the average of duplicate technical replicates from an individual animal. Data represent mean ± SEM of 5 (WT) or 10 (Il4ra−/−) independent mice. p value (*p < 0.05 and **p < 0.01) was calculated by two-tailed unpaired parametric t test.
(F–L) Triamcinolone effects on the expression of Il17a (F), Il4 (G), Il13 (H), and AMP genes (I–K) and survival of S. aureus for 48 h in WT mice pretreated with MC903 or vehicle (L). Each dot represents the average of duplicate technical replicates from an individual animal. Data represent mean ± SEM of 5–6 biological replicates from independent mice as individually shown. p value (*p < 0.05, **p < 0.01, and ***p < 0.001) was calculated by two-tailed Mann-Whitney U test (F–K) or two-tailed unpaired parametric t test (L).
(M) Illustration of the host antimicrobial peptide response to S. aureus colonization in presence or absence of Th2 inflammation and in WT or Il4ra−/− skin.