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. 2024 Apr;90(4):749-758.
doi: 10.1016/j.jaad.2023.11.048. Epub 2023 Dec 3.

Tape strips detect molecular alterations and cutaneous biomarkers in skin of patients with hidradenitis suppurativa

Affiliations

Tape strips detect molecular alterations and cutaneous biomarkers in skin of patients with hidradenitis suppurativa

Kristina Navrazhina et al. J Am Acad Dermatol. 2024 Apr.

Abstract

Background: Hidradenitis suppurativa (HS) has a high unmet need for better treatments. Biopsies are considered the gold standard for studying molecular alterations in skin. A reproducible, minimally invasive approach is needed for longitudinal monitoring in trials and in pediatric populations.

Objective: To determine whether skin tape strips can detect molecular alterations in HS and identify biomarkers of disease activity.

Methods: We performed RNA sequencing on tape strips collected from lesional and healthy-appearing (nonlesional) HS skin (n = 22) and healthy controls (n = 21). We correlated the expression of skin biomarkers between tape strips and a previously published gene-signature of HS biopsies.

Results: Tape strips detected upregulation of known HS biomarkers (eg, Interleukin[IL]-17A) in nonlesional and/or lesional skin and also identified novel clinically actionable targets, including OX40 and JAK3. The expression of Th17 and tumor necrosis factor-α pathways were highly correlated between tape strips and biopsies. HS clinical severity was significantly associated with expression of biomarkers (eg tumor necrosis factor-α , IL-17 A/F, OX40, JAK1-3, IL-4R) in HS lesional and/or nonlesional skin.

Limitations: Sample size. Tape stripping is limited in depth.

Conclusion: This study validates tape strips as a minimally-invasive approach to identify cutaneous biomarkers in HS. This provides a novel avenue for monitoring treatment efficacy and a potential step toward individualized therapy in HS.

Keywords: IL-17; RNA-sequencing; TNF; biomarkers; hidradenitis suppurativa; inflammation; tape strips; transcriptome.

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Conflict of interest statement

Conflicts of interest KN, HH, MM, EA, MK, MM, DGS, SB, SCW, SG, JCR have no conflicts to disclose. SK is an employee of Mount Sinai and a consultant for AbbVie, Eli Lilly, Glenmark, Ichnos Sciences, Janssen, and Novartis. She serves on the Advisory Boards for Eli Lilly, Glenmark, Ichnos Sciences, Janssen, Abbvie, Argenx, Regeneron-Sanofi, Novartis, and UCB. She has received research funds from Pfizer, AbbVie, BMS, Incyte, Galderma and Acelyrin, and speaker bureau for AbbVie, Regeneron-Sanofi, Lilly, UCB, Janssen, Arcutis and Leo. ABG has received honoraria as an advisory board member and consultant for Amgen, AnaptypsBio, Avotres Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Dice Therapeutics, Eli Lilly, Janssen, Novartis, Sanofi, UCB, and Xbiotech and has received research/educational grants from AnaptypsBio, Moonlake Immunotherapeutics AG, Novartis, Bristol-Myers Squibb, and UCB Pharma (all paid to Mount Sinai School of Medicine). JGK has acted as a consultant for and/or received honoraria from AbbVie, Aclaris, Allergan, Almirall, Amgen, Arena, Aristea, Asana, Aurigene, Biogen Idec, Boehringer Ingelheim, Bristol-Myers Squibb, Escalier, Galapagos, Janssen, Lilly, MoonLake Immunotherapeutics, Nimbus, Novartis, Pfizer, Sanofi, Sienna Biopharmaceuticals, Sun Pharma, Target-Derm, UCB, Valeant, and Ventyx. James Krueger has received grant support (to The Rockefeller University) from AbbVie, Akros, Allergan, Amgen, Avillion, Biogen, Botanix, Boehringer Ingelheim, Bristol-Myers Squibb, Exicure, Innovaderm, Incyte, Janssen, Kyowa Kirin, Lilly, Nimbus Lackshmi, Novan, Novartis, PAREXEL, Pfizer, Regeneron, UCB, and Vitae Pharmaceuticals. EGY has served as a consultant for AbbVie, Amgen, Allergan, Asana Bioscience, Celgene, Concert, Dermira, DS Biopharma, Escalier, Galderma, Glenmark, Kyowa Kirin, LEO Pharmaceuticals, Lilly, Mitsubishi Tanabe, Novartis, Pfizer, Regeneron, Sanofi, and Union Therapeutics; a member of advisory boards of Allergan, Asana Bioscience, Celgene, DBV, Dermavant, Dermira, Escalier, Galderma, Glenmark, Kyowa Kirin, LEO Pharma, Lilly, Novartis, Pfizer, Regeneron, and Sanofi; and a recipient of research grants from AbbVie, AnaptysBio, AntibioTx, Asana Bioscience, Boehringer-Ingelheim, Celgene, DBV, Dermavant, DS Biopharma, Galderma, Glenmark, Innovaderm, Janssen Biotech, Kiniksa Pharma, LEO Pharmaceuticals, Lilly, Medimmune, Sienna Biopharmaceuticals, Novan, Novartis, Ralexar, Regeneron, Pfizer, UCB, and Union Therapeutics.

Figures

Fig 1.
Fig 1.
Summary of differentially expressed genes (DEGs). Volcano plot denoting significantly down (blue) or up (red) regulated DEGs between lesional (LS) hidradenitis suppurativa (HS) and healthy control skin. DEGs were defined with absolute fold change (FCH ) ≥1.5 and false discovery rate (FDR) < 0.1. The log2 fold change is illustrated on the x-axis and −log10 adjusted P value on the y axis.
Fig 2.
Fig 2.
Spearman correlation of TNF-α-associated gene set between tape strip and punch biopsies. Scatterplot compares relative log2 fold-changes (FCH) of expression of genes within the TNF-α gene-set in lesional (LS) hidradenitis suppurativa (HS) skin detected by tape strips (x axis) versus biopsies from a previously published whole-tissue biopsies transcriptome. Circle diameters are directly proportional to log2FCH of gene expression.
Fig 3.
Fig 3.
Interleukin (IL)-17 pathway signature. Bar plot depicts individual z-scores within the IL-17 gene set variation analysis (GSVA) from tape-stripped control healthy volunteer skin (HV) and hidradenitis suppurativa (HS) nonlesional (NL), lesional (LS) and error bars represent standard error of the mean. Red stars indicate significance of comparison between NL and LS skin with HV: *P < .05; **P < .01; ***P < .001.

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