L24
Proteomic Profiling of Atopic Dermatitis, Psoriasis, and Contact Dermatitis Patients
Sunday, March 6, 2016
South Exhibit Hall H (Convention Center)
Jingya Wang, Mayte Suarez-Farinas, PhD, Yeriel Estrada, James G. Krueger, MD PhD, Melissa Parker, Emma Guttman-Yassky, MD PhD, Michael D. Howell, PhD
Rationale: Atopic dermatitis (AD), psoriasis (PS), and contact dermatitis (CD) are common inflammatory skin diseases characterized by significant barrier disruption and systemic inflammation.  Transcriptomic profiling has identified unique epidermal signatures as well as common inflammatory pathways.  Given the systemic nature of the diseases, this study profiled the proteomic signatures in serum from subjects with AD, PS, and CD compared to healthy donor controls.

Methods: Serum was collected from 20 subjects with moderate-to-severe AD, 20 subjects with CD, 12 subjects with moderate-to-severe PS, and 10 healthy controls with no history of skin disease.  Protein expression was evaluated by SOMAscan™, Singulex®, and multiplex technology.  Expression in AD, CD, and PS serum was compared to healthy controls for statistical significance (fold change ≥ 1.5 and false discovery rate < 0.05) and lists compared between diseases to identify unique proteomic signatures.  

Results: This study identified 7 proteins (Up Regulated: C5a, PARC, LBP, CRP, ILT-4; Down Regulated: CAMK2B, Carbonic anhydrase 6) that were similarly modulated in all inflammatory skin diseases compared to healthy controls. Additional comparisons with serum from healthy controls revealed significant modulations in a total of 25, 5, and 64 proteins in subjects with AD, PS, and CD, respectively. Protein signatures were further refined by comparing between inflammatory skin diseases.  This resulted in a unique signature of increased IgE, CCL17/TARC, and CCL22/MDC in AD; which significantly correlated (p<0.05) with disease severity.  

Conclusions: This study suggests unique proteomic signatures in the sera may potentially distinguish between inflammatory skin diseases despite similar epidermal barrier disruption and epithelial inflammation.