Gene expression profiling of filaggrin-insufficient keratinocytes exposed to inflammatory mediators and allergens

Loss-of-function mutations in the filaggrin gene are heavily associated with the incidence and severity of atopic dermatitis. Moreover, filaggrin insufficiency in epidermal keratinocytes can lead to persistent allergic inflammation and an associated immune response suggesting a role for this protein in regulation of immunity. Here, we investigate how filaggrin insufficiency affects the gene expression pattern in a filaggrin-insufficient (shFLG) keratinocyte cell line HaCaT in response to stimulation with various inflammatory mediators and allergens. Untreated shC and shFLG cells were used as controls for their corresponding conditions. Treatment with the following compounds was performed: histamine, amphiregulin, IFNy, IL-4/IL-13, cysteine, derp1/cysteine, derp2; concentrations for every compound were provided below in sample description. Biological triplicates of every condition were generated. A total of 48 samples were analyzed. The filaggrin gene (FLG) in the HaCaT cell line was silenced by shRNA delivered to the cells using lentiviral particles. Scrambled RNA was used for generation of control (shC) cells.