The bacterial diversity in lesional and nonlesional skin of patients with psoriasis (PsO) with or without psoriatic arthritis (PsA) was significantly lower than that of healthy control skin, based on data from 74 individuals.
Previous studies in humans and animals have suggested that microbes play a role in PsO pathogenesis, but microbial analyses of PsA are lacking, wrote Alba Boix-Amorós, PhD, of the Icahn School of Medicine at Mount Sinai, New York City, and colleagues.
“The passage from PsO to PsA may, in part, be driven by microbial triggers, which deserves further investigation,” they wrote.
In a study published in Annals of the Rheumatic Diseases, the researchers recruited 23 patients with PsO and 31 with PsA from the dermatology and rheumatology clinics at the NYU Grossman School of Medicine/NYU Langone Health in New York City. An additional 20 healthy individuals with no history of PsA or PsO were recruited from within NYU to serve as controls. All participants were aged 18 years and older, and more than 75% were white. Males made up 65.4%, 47.8%, and 55.0% of the PsA, PsO, and control groups, respectively.
The researchers collected skin swabs from lesional and nonlesional skin of individuals with PsO and PsA and from the upper and lower extremities of the healthy controls. The microbiota analysis included 148 samples that were analyzed using 16S rRNA sequencing.
The microbiome diversity was significantly greater in healthy skin, compared with lesional and nonlesional psoriatic skin (P < .05 for both). Specifically, levels of Cutibacterium and Kocuria were significantly higher in healthy skin than in psoriatic skin (P = .016 and P = .011, respectively), while psoriatic skin showed higher levels of Staphylococcus.
No significant microbiome differences were noted between lesional and nonlesional PsO and PsA samples. The finding that the microbiome of nonlesional psoriatic skin was more similar to lesional psoriatic skin than to healthy skin was unexpected, and suggests the development of microbial dysbiosis in psoriatic skin independent of the presence of lesions, the researchers wrote.
The researchers also found that levels of Corynebacterium in nonlesional PsA samples were significantly elevated, compared with nonlesional PsO samples (P < .05), which suggests a possible role for the microbe as a biomarker for disease progression, the researchers said.
“One important application of these data is the potential development of therapeutic options for the treatment of psoriatic disease and/or the prevention of PsA,” the researchers wrote in their discussion.
The findings were limited by several factors, including the combination of samples from upper and lower extremities and the exclusion of data from the scalp, the researchers noted. Other limitations included the use of only 16S rRNA gene sequencing, which presents a less comprehensive view of the microbiome, they said.
However, the results support the role of the skin microbiome in psoriasis pathogenesis, with details on microbiota across the psoriatic disease spectrum, they said.
The study received no outside funding. Boix-Amorós had no financial conflicts to disclose. Several coauthors disclosed financial relationships with pharmaceutical companies including Janssen, AbbVie, Bristol-Myers Squibb, Johnson & Johnson, Eli Lilly, Pfizer, Novartis, Sanofi, and UCB.
This article originally appeared on MDedge.com, part of the Medscape Professional Network.
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