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Transcriptome patterns in hidradenitis suppurativa: support for the role of antimicrobial peptides and interferon pathways in disease pathogenesis
Author(s) -
Shanmugam V. K.,
Jones D.,
McNish S.,
Bendall M. L.,
Crandall K. A.
Publication year - 2019
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/ced.13959
Subject(s) - hidradenitis suppurativa , transcriptome , downregulation and upregulation , pathogenesis , antimicrobial peptides , medicine , immunology , immune system , interferon , gene expression , biology , microbiology and biotechnology , gene , disease , antimicrobial , genetics
Summary Background Hidradenitis suppurativa ( HS ) is a recurrent inflammatory disease of the apocrine sweat glands. Immune dysregulation probably contributes to the pathogenesis of HS . Aim To harness mRNA expression arrays to investigate the transcriptome profile in HS compared with control skin. Methods Illumina ® Human HT ‐12 v4 Expression BeadChips were used to measure mRNA expression in skin samples from HS ( n = 10) and abdominoplasty ( n = 11) skin specimens. Differentially expressed genes were detected by fitting genewise linear models to the normalized expression data and then modelling using the web‐based software Ingenuity ® Pathway Analysis. Results The antimicrobial peptide Dermcidin and the cytokine regulator interleukin (IL)‐37 were both significantly downregulated in the HS specimens (Dermcidin expression log ratio −3.93, expression P = 0.04; IL ‐37 expression log ratio −3.29, expression P < 0.001). Pathway analysis revealed the interferon‐signalling pathway, leucocyte extravasation pathway, T helper 1 and 2 pathways and nuclear factor of activated T cells as the top‐five upregulated pathways in the HS samples. Conclusion Evaluation of transcriptome patterns in HS compared with normal skin demonstrated downregulation of the antimicrobial peptide Dermcidin and the innate immune regulator IL‐37, as well as upregulation of interferon pathways and pathways of leucocyte activation.