In people with eczema (atopic dermatitis), the skin’s natural antimicrobial peptide LL‑37 isn’t always low – newer studies show it can be as high or higher than in healthy skin. However, these patients still get frequent Staph infections, meaning the peptide either isn’t working well enough or other factors (like a leaky barrier) are to blame. Raising LL‑37 levels and fixing the skin’s barrier might help the skin fight germs better.

Keratinocytes represent the major cell population in the epithelial skin barrier and actively participate in innate immune responses by recognizing pathogenic microorganisms, followed by a fine-tuned production of cytokines, chemokines and antimicrobial peptides or proteins (AMPs). Patients with atopic dermatitis (AD) suffer from a defective permeability barrier which favors pathogen infection indicating that the permeability and antimicrobial barrier functions are interdependent. Several early studies showed that the inducible AMPs LL-37, HBD-2 and HBD-3 are expressed at lower levels in atopic skin compared to psoriatic skin. However, recent data indicate that AMP induction is not compromised in AD patients and that several AMPs are expressed at significantly higher amounts in AD compared to healthy skin. AD patients have an increased susceptibility to Staphylococcus aureus skin infection suggesting that AMP levels expressed by keratinocytes of AD patients might not be sufficient to combat pathogenic skin infection or that AMP function is disturbed. Increasing AMP expression in AD skin and repairing the skin barrier defect might have a therapeutic effect in AD patients enabling the skin to mount an enhanced response to pathogens.