Cathelicidin expression in the pathogenesis of atopic dermatitis and the therapeutic potential of vitamin D

Abstract

Atopic dermatitis (AD) is a common inflammatory skin condition. Emerging evidence indicates that alterations in the cutaneous expression of the antimicrobial peptide cathelicidin contribute to AD pathogenesis, including weakened skin barrier (SB) function, and Staphylococcus aureus (SA) colonization. Cathelicidin expression is vitamin D (VD)–dependent and low VD, highly prevalent in AD populations, may impede cathelicidin induction. This review investigates the pathophysiological mechanisms linking cathelicidin expression with SB function and SA colonization/infection, and the impact of VD as a nutritional intervention to target cathelicidin expression, SB function, and SA colonization/infection to inform AD management in clinical practice. We hypothesize that low VD concentrations contribute to reduced cathelicidin expression and the development and/or exacerbation of AD, and interventions to increase serum VD concentrations may upregulate cathelicidin expression and ameliorate AD pathogenesis. A systematic literature search was performed. Sixty-eight peer-reviewed papers were accepted, critically appraised, and summarized in a narrative analysis. Our findings indicate: (1) cathelicidin has a role in SB function and anti-SA activity and (2) VD supplementation (VDS) at doses of 1000–2000 IU/day for 1 to 3 months increases cathelicidin expression and reduces SA abundance and AD severity in individuals with low serum VD. There is no evidence to support the use of VDS in individuals with sufficient serum VD. The results support the use of VDS at 1000–2000 IU/day for 3 months to ameliorate AD pathophysiology when serum VD concentrations are within deficiency/insufficiency ranges. Further clinical research is required to establish optimal dosage and duration for VDS interventions.