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Alterations in the cutaneous microbiome of patients with psoriasis and psoriatic arthritis reveal similarities between non-lesional and lesional skin
  1. Alba Boix-Amorós1,
  2. Michelle H Badri2,
  3. Julia Manasson3,
  4. Rebecca B Blank3,
  5. Rebecca H Haberman3,
  6. Andrea L Neimann4,
  7. Parvathy V Girija3,
  8. Anthony Jimenez Hernandez3,
  9. Adriana Heguy5,6,
  10. Sergei B Koralov6,
  11. Richard Bonneau2,7,
  12. Jose C Clemente1,
  13. Jose U Scher3
  1. 1Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA
  2. 2Department of Biology, New York University, New York, New York, USA
  3. 3Division of Rheumatology, Department of Medicine and Psoriatic Arthritis Center, New York University Grossman School of Medicine, New York, New York, USA
  4. 4Ronald O. Perelman Department of Dermatology, New York University Grossman School of Medicine, New York, New York, USA
  5. 5NYU Langone Health Genome Technology Center, Department of Pathology, New York University Grossman School of Medicine, New York, New York, USA
  6. 6Department of Pathology, New York University Grossman School of Medicine, New York, New York, USA
  7. 7Center for Computational Biology, Flatiron Institute, Simons Foundation, New York, New York, USA
  1. Correspondence to Dr Jose U Scher, Division of Rheumatology, Department of Medicine and Psoriatic Arthritis Center, New York University Grossman School of Medicine, New York, New York 10016, USA; jose.scher{at}nyulangone.org

Abstract

Objectives To investigate the cutaneous microbiome spanning the entire psoriatic disease spectrum, and to evaluate distinguishing features of psoriasis (PsO) and psoriatic arthritis (PsA).

Methods Skin swabs were collected from upper and lower extremities of healthy individuals and patients with PsO and PsA. Psoriatic patients contributed both lesional (L) and contralateral non-lesional (NL) samples. Microbiota were analysed using 16S rRNA sequencing.

Results Compared with healthy skin, alpha diversity in psoriatic NL and L skin was significantly reduced (p<0.05) and samples clustered separately in plots of beta diversity (p<0.05). Kocuria and Cutibacterium were enriched in healthy subjects, while Staphylococcus was enriched in psoriatic disease. Microbe–microbe association networks revealed a higher degree of similarity between psoriatic NL and L skin compared with healthy skin despite the absence of clinically evident inflammation. Moreover, the relative abundance of Corynebacterium was higher in NL PsA samples compared with NL PsO samples (p<0.05), potentially serving as a biomarker for disease progression.

Conclusions These findings show differences in diversity, bacterial composition and microbe–microbe interactions between healthy and psoriatic skin, both L and NL. We further identified bacterial biomarkers that differentiate disease phenotypes, which could potentially aid in predicting the transition from PsO to PsA.

  • Arthritis, Psoriatic
  • Epidemiology
  • Autoimmune Diseases

Data availability statement

Data are available in a public, open access repository. All sequence data will be made publicly available on publication at the NIH Sequence Read Archive (https://www.ncbi.nlm.nih.gov/sra). Additionally, code that was used to perform computational analyses in this manuscript will be made available at https://github.com/scher-lab.

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Data availability statement

Data are available in a public, open access repository. All sequence data will be made publicly available on publication at the NIH Sequence Read Archive (https://www.ncbi.nlm.nih.gov/sra). Additionally, code that was used to perform computational analyses in this manuscript will be made available at https://github.com/scher-lab.

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Footnotes

  • AB-A, MHB and JM are joint first authors.

  • RB, JCC and JUS are joint senior authors.

  • Handling editor Josef S Smolen

  • Correction notice This article has been corrected since it published Online First. The name has been updated for author Sergei Koralov and the funding statement added.

  • Contributors AB-A, MHB, JM, SK, RB, RHH, JCC and JUS designed the study. RHH, AJ and PvG collected samples and conducted experiments. AB-A, MHB, JM, JCC and JUS conducted data analysis and produced the figures and tables. AB-A, MHB, JM, RB, JCC and JUS wrote the manuscript. AB-A, MHB and JB are joint first authors. RB, JCC and JUS are joint senior authors. All authors approved the final version of the article.

    JUS acts as guarantor and accepts full responsibility for the work, the conduct of the study, had access to the data, and controlled the decision to publish.

  • Funding National Psoriasis Foundation Early Career Grant (PI: Manasson), NIH/NIAMS R01AR074500 (PI: Scher, Co-I: Manasson), NIH/NIAMS T32 AR069515 (PI: Buyon, Trainee: Manasson), Rheumatology Research Foundation Investigator Award (PI: Manasson), Psoriatic Arthritis Center (PI: Scher), Riley Family Foundation (PI: Scher), Beatrice Snyder Foundation (PI: Scher), Cancer Center Support Grant P30CA016087 at the Laura and Isaac Perlmutter Cancer Center (support for NYU Genome Technology Center), National Psoriasis Foundation (PI: Koralov and Scher), LEO Foundation (PI: Koralov), Colton Center for Autoimmunity Pilot Grant (PI: Koralov and Scher), National Psoriasis Foundation Early Career Grant (PI: Manasson), NIH/NIAMS R01AR074500 (PI: Scher, Co-I: Manasson), NIH/NIAMS T32 AR069515 (PI: Buyon, Trainee: Manasson), Rheumatology Research Foundation Investigator Award (PI: Manasson), Psoriatic Arthritis Center (PI: Scher), Riley Family Foundation (PI: Scher), Beatrice Snyder Foundation (PI: Scher), Cancer Center Support Grant P30CA016087 at the Laura and Isaac Perlmutter Cancer Center (support for NYU Genome Technology Center), National Psoriasis Foundation (PI: Koralov and Scher), LEO Foundation (PI: Koralov), Colton Center for Autoimmunity Pilot Grant (PI: Koralov and Scher).

  • Competing interests RHH: received consulting fees from Janssen ALN: served as a consultant for Janssen, UCB, AbbVie and Bristol-Myers Squibb; has an immediate family member who owns shares of stock in J&J, Eli Lilly, AbbVie and Pfizer JUS: served as a consultant for Janssen, Abbvie, Novartis, Sanofi, UCB and BMS.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.