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18245 Polymicrobial composition of psoriatic skin

2020; Elsevier BV; Volume: 83; Issue: 6 Linguagem: Inglês

10.1016/j.jaad.2020.06.466

1097-6787

Kory P. Schrom, CWRU Iman Salem, Sherman Chu, Mauricio Retuerto, Seunghee Margevicius, Ming Li, Neil J. Korman, Mahmoud Ghannoum, Thomas S. McCormick, Kevin D. Cooper,

Biosimilars and Bioanalytical Methods

Psoriasis is a chronic inflammatory disease that affects ∼2% of the population and is characterized by immune-mediated, keratinocyte hyperproliferation. Recently, the importance of the microbiome in psoriasis has been demonstrated using high throughput DNA-sequencing technologies. We report here associations between disease severity and the bacterial (ie bacteriome) and fungal (ie mycobiome) components of the cutaneous microbiome. Skin swab samples were obtained from involved and uninvolved psoriatic plaques of 67 patients. Disease severity was assessed by body surface area (BSA). Amplification of the 16S (bacterial) and ITS1 region (fungal) genes was performed using 16S 515f-804r and ITS1f and ITS2r primers, respectively. The targeted amplicons were sequenced using an Ion Torrent S5 system. Relative abundance was determined using non-parametric comparisons (Wilcoxon rank-sum test; Kolmogorov-Smirnov test). A positive correlation between disease severity and increased relative abundance of Serratia marcescens, Escherichia coli, and Candida albicans (P = .0360, 0.05, 0.0094, respectively) was observed. Higher C. albicans abundance has been linked to an altered immune response triggering inflammation in psoriasis. Healthy skin is typically resistant to E. coli owing to production of antimicrobial peptides by keratinocytes. Interestingly, an increased abundance of C. albicans, E. coli, and S. marcescens has also been described in the gut of patients with Crohn disease, an autoimmune disorder linked with psoriasis. Taken together, this data suggests that abundant organisms in psoriatic lesions increase the likelihood of polymicrobial interactions in the skin that may affect host immune responses.