The Follicular Skin Microbiome in Patients With Hidradenitis Suppurativa and Healthy ControlsOriginal paper
What was studied?
This case-control study investigated the follicular skin microbiome in hidradenitis suppurativa (HS), a chronic inflammatory follicular skin disease of enigmatic pathogenesis. Punch biopsy specimens were profiled by next-generation sequencing to compare the microbial communities of HS skin with those of healthy controls.
Who was studied?
The microbiome was characterized in 30 patients with HS (mean age 46.9 years, 63% female) and 24 healthy controls (mean age 32.2 years, 54% female) recruited at Zealand University Hospital in Roskilde, Denmark, between October 2014 and August 2016, with no participant having taken systemic or topical antibiotics within the prior month. HS biopsies were taken from lesional skin (axilla or groin) and nonlesional skin, control biopsies from the axilla only, and each biopsied nodule contained at least one visible hair follicle. Sequencing targeted the bacterial 16S and eukaryotic 18S ribosomal RNA genes.
What were the most important findings?
The skin microbiome in HS differed significantly from that of healthy controls in both lesional and nonlesional skin. Five microbiome types were identified: Corynebacterium species (type I), Acinetobacter and Moraxella species (type II), Staphylococcus epidermidis (type III), Porphyromonas and Peptoniphilus species (type IV), and Propionibacterium acnes (type V); HS lesional skin consisted predominantly of type I or type IV, and type IV was not detected in any healthy control. Several taxa, including Propionibacterium, showed significantly higher relative abundance in healthy controls than in HS skin.
What are the greatest implications of this study?
The authors conclude that these findings suggest a link between a dysbiotic cutaneous microbiome and HS, with depletion of Propionibacterium potentially contributing to the pathogenesis. Because this is an observational case-control design, the results indicate association rather than causation, and the older age of HS patients relative to controls is a potential confounder.