Hidradenitis suppurativa presents a methylome dysregulation capable to explain the pro‐inflammatory microenvironment: Are these DNA methylations potential therapeutic targets?

Author:

Radhakrishna Uppala1ORCID,Ratnamala Uppala2,Jhala Devendrasinh D.23ORCID,Uppala Lavanya V.4,Vedangi Aaren5,Patel Maulikkumar6,Vadsaria Nikita6,Shah Sushma7,Saiyed Nazia2,Rawal Rakesh M.4,Mercuri Santo Raffaele89,Jemec Gregor B. E.10,Damiani Giovanni891112

Affiliation:

1. Department of Obstetrics and Gynaecology Oakland University William Beaumont School of Medicine Royal Oak Michigan USA

2. Department of Life Sciences, School of Sciences Gujarat University Ahmedabad India

3. Department of Zoology School of Sciences, Gujarat University Ahmedabad India

4. College of Information Science & Technology The University of Nebraska at Omaha, Peter Kiewit Institute Omaha Nebraska USA

5. Department of Clinical Research KIMS ICON Hospital, A Unit of ICON Krishi Institute Medical Sciences Visakhapatnam India

6. Bioinformatics Gujarat University Ahmedabad India

7. Department of Obstetrics and Gynaecology B.J. Medical College Ahmedabad India

8. Unit of Clinical Dermatology Università Vita‐Salute San Raffaele Milan Italy

9. Italian Center of Precisione Medicine and Chronic Inflammation Milan Italy

10. Department of Dermatology Zealand University Hospital Roskilde Denmark

11. Clinical Dermatology Case Western Reserve University Cleveland Ohio USA

12. Young Dermatologists Italian Network Milan Italy

Abstract

AbstractBackgroundHidradenitis suppurativa (HS) is a chronic, systemic, inflammatory skin condition with elusive pathogenesis that affects therapeutic intervention directly.ObjectiveTo characterize epigenetic variations in cytokines genes contributing to HS.MethodsEpigenome‐wide DNA methylation profiling with the Illumina Epic array was performed on blood DNA samples from 24 HS patients and 24 age‐ and sex‐matched controls to explore DNA methylation changes in cytokine genes.ResultsWe identified 170 cytokine genes including 27 hypermethylated CpG sites and 143 genes with hypomethylated sites respectively. Hypermethylated genes, including LIF, HLA‐DRB1, HLA‐G, MTOR, FADD, TGFB3, MALAT1 and CCL28; hypomethylated genes, including NCSTN, SMAD3, IGF1R, IL1F9, NOD2, NOD1, YY1, DLL1 and BCL2 may contribute to the pathogenesis of HS. These genes were enriched in the 117 different pathways (FDR p‐values ≤ 0.05), including IL‐4/IL‐13 pathways and Wnt/β‐catenin signalling.ConclusionsThe lack of wound healing, microbiome dysbiosis and increased tumour susceptibility are all sustained by these dysfunctional methylomes, hopefully, capable to be targeted in the next future. Since methylome describes and summarizes genetic and environmental contributions, these data may represent a further step towards a feasible precision medicine also for HS patients.

Publisher

Wiley

Subject

Infectious Diseases,Dermatology

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