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

Clinical and Experimental Dermatology, ISSN: 1365-2230, Vol: 44, Issue: 8, Page: 882-892
2019
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  • 26
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  • 46
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  • 4
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Alterations in pathway activation found in hidradenitis suppurativa

Biological pathways are disrupted among patients with hidradenitis suppurativa, which suggests that inflammatory pathways, pathways of leucocyte activation and signaling, and innate immune responses require more study, according to researchers. “This highlights the importance of the immune system in [hidradenitis suppurativa] and identifies deficient or suppressed antimicrobial peptide levels as a

Article Description

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.

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