Fig. 5
TRAF1-deficiency promotes CXCL1 production with C. albicans infection. a. Traf1−/− mice (n = 3) and WT controls (n = 2) were infected with C. albicans (1 × 107 CFU) or PBS and analyzed for gene expression within the skin tissue 3 days post-infection by qPCR. Results were reported as fold change normalized to the expression of β-actin and relative to PBS control. PBS group, the control group; CA group, the c. albicans infection group. b. Traf1−/− and WT BMDMs pretreated with IL-4 (10 ng/ml) O/N were unstimulated or stimulated with HK-CA (MOI = 5) for 6 h and the expression of Cxcl1, Cxcl2, Il6, Ilβ, Tnfα, iNOS was evaluated by qPCR. Results were reported as fold change normalized to the expression of β-actin and relative to untreated control. c. Traf1−/− and WT BMDMs pretreated with IL-4 (10 ng/ml) O/N were stimulated with HK-CA (MOI = 5) or not for 24 h and the protein levels of CXCL1 were evaluated by ELISA. d. CTRL and sg-Traf1 HaCaT cells were either stimulated or unstimulated with TNFα (20 μg/ml) plus IL17A (50 μg/ml) for 9 h, and the expression of Cxcl8, S100A9, BD2 was evaluated by qPCR. Results were reported as fold change normalized to the expression of β-actin and relative to untreated control. Data are shown as mean ± SEM and are representative of at least two experiments performed in triplicate. Data were analyzed using the unpaired, two-tailed, Student’s t-test. Values of p below 0.05 represented a statistically significant difference