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Transcriptome patterns in hidradenitis suppurativa: support for the role of antimicrobial peptides and interferon pathways in disease pathogenesis

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. Met...

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Bibliographic Details
Published in:Clinical and experimental dermatology 2019-12, Vol.44 (8), p.882-892
Main Authors: Shanmugam, V. K., Jones, D., McNish, S., Bendall, M. L., Crandall, K. A.
Format: Article
Language:English
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Summary: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® HumanHT‐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.
ISSN:0307-6938
1365-2230
DOI:10.1111/ced.13959