The study found that a skin yeast called Malassezia sympodialis makes immune cells (dendritic cells) release more of the natural antibiotic peptide LL‑37, but only in people with severe atopic eczema. Healthy people’s cells didn’t show this increase.

Atopic eczema (AE) is a multifactorial disease, which has increased in prevalence. The skin-colonizing yeast Malasezzia sympodialis can induce IgE- and T-cell reactivity in patients with AE. LL-37 is an endogenous peptide antibiotic belonging to the cathelicidin family. The aim of this study was to examine whether exposure to M. sympodialis would affect the expression of LL-37 in dendritic cells. The presence of LL-37 was analyzed in monocyte-derived dendritic cells (MDDCs) generated from healthy individuals and patients with AE by Western blotting and the corresponding cDNA by real-time quantitative RT-PCR. Antibacterial activity was measured with an inhibition zone assay in fractions after reverse phase chromatography. For the first time we here present data, showing that LL-37 is produced by MDDCs. Notably, the secretion of LL-37 was substantially enhanced in M. sympodialis-exposed MDDCs generated from patients with a high degree of eczema, as measured by SCORAD, compared to healthy controls and patients with a low SCORAD. The relative expression of LL-37 transcript in MDDCs generated from patients was up-regulated after 1 h of exposure to M. sympodialis and declined gradually at the time points analyzed, whereas the transcription was unaffected in the MDDCs of healthy controls. Our results suggest that M. sympodialis can trigger the innate immune response differently in patients with AE and healthy individuals. The enhanced LL-37 secretion from the MDDCs in the patients with AE may reflect the severity of their inflammatory response to M. sympodialis.