Primary alterations during the development of hidradenitis suppurativa

Dajnoki, Zsolt; Somogyi, Orsolya; Medgyesi, Barbara; Jenei, Adrienn; Szabó, Lilla; Gáspár, Krisztián; Hendrik, Zoltán; Gergely, Pál; Imre, D.; Póliska, Szilárd; Törőcsik, Dániel; Zouboulis, Christos C.; Prens, E.P.; Kapitány, Anikó; Szegedi, Andrea

doi:10.1111/jdv.17779

Cited by 25 publications

(30 citation statements)

References 24 publications

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“…It is feasible, that this keratinocytic activation partly results from sweatderived IFN-γ. Likewise, MCP-1 (also known as CCL2) has recently been shown as elevated in lesional and nonlesional HS epidermis ( 34 ) and could also contribute to the proinflamatory milieu.…”

Section: Discussionmentioning

confidence: 99%

Hidradenitis Suppurativa: Absence of Hyperhidrosis but Presence of a Proinflammatory Signature in Patients’ Sweat

Frings

Roth²,

Gläsel³

et al. 2022

Acta Derm Venereol

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The role of sweat glands in hidradenitis suppurativa has been largely neglected, despite the fact that its original designation, as “hidrosadénite phlegmoneuse”, implied an inflammatory malfunction of the apocrine sweat glands as the underlying pathogenic driver. The aim of this study was to evaluate the role of apocrine sweat glands with respect to the proinflammatory environment of hidradenitis suppurativa. Therefore, gravimetric assessment and multiplex cytokine assays from sweat obtained from patients with hidradenitis suppurativa along with immunofluorescence cytokine/chemokine analysis of lesional apocrine glands-bearing hidradenitis suppurativa skin were performed. Gravimetric assessment of 17 patients with hidradenitis suppurativa revealed that the condition is not associated with hyperhidrosis. However, patients seem to be more affected by subjective sweating. The current data identified a complex proinflammatory signature in hidradenitis suppurativa sweat characterized by a significant upregulation of monocyte chemoattractant protein-1, interleukin-8 (CXCL8), and interferon-γ. In agreement with this, a strong in situ expression of these mediators could be observed in apocrine glands of lesional hidradenitis suppurativa skin. These data shed new light on the proinflammatory capacity of apocrine sweat glands in hidradenitis suppurativa, which may lead to reconsideration of the role of sweat glands in hidradenitis suppurativa pathology.

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Section: Discussionmentioning

confidence: 99%

Hidradenitis Suppurativa: Absence of Hyperhidrosis but Presence of a Proinflammatory Signature in Patients’ Sweat

Frings

Roth²,

Gläsel³

et al. 2022

Acta Derm Venereol

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show abstract

“…The levels of pro-inflammatory cytokines IL-1β, TNFα, IL-8, IL-28, IL-32, IL-23, the anti-inflammatory cytokine IL-10, and IL-6 (with both pro-inflammatory and anti-inflammatory roles) were also raised in HS lesional and perilesional skin, showing a positive correlation with disease severity 28,30,32,[48][49][50][51] . This presence of pro-inflammatory cytokines beyond HS lesions could explain the high recurrence rates after surgical excision, highlighting the importance of systemic inflammation in the progression of the disease.…”

Section: Hla-ii Alleles (mentioning

confidence: 97%

“…Innate immunity is crucial for developing HS 28,29 . This was demonstrated by the up-regulation of messenger RNA (mRNA) levels of antimicrobial peptides (AMP) 30 and proteins such as human-β-defensin 1 (hBD-1), hBD-2, and hBD-3, cathelicidin (LL-37), ribonuclease 7 (RNase 7), and nucleotide-binding oligomerization…”

Section: Immunitymentioning

confidence: 99%

“…There is some evidence concerning up-regulation of serum biomarkers. Nevertheless, only high levels of C-reactive protein are consistent among patients with HS [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] . AMP: antimicrobial peptides; hBD: human-β-defensin; LL-37: cathelicidin; RNAase 7; ribonuclease 7; NOD2: nucleotide-binding oligomerization domain-containing 2; ICAM: intercellular adhesion molecule; TGFβ: tumor growth factor β; IL: interleukin; CRP: C-reactive protein; LCN2: lipocalin 2; c5a: complement factor C5a; ESR: erythrocyte sedimentation rate.…”

Section: Immunitymentioning

confidence: 99%

“…Hidradenitis suppurativa is characterized by inappropriate AMP secretion, and proinflammatory cytokine dysregulation 29,30,32,35 . Increased activity of dendritic cells and T cells cause keratinocyte hyperplasia via IL-23, IL-12, and Th17 immune response 30,47 .…”

Section: Conflicts Of Interestmentioning

confidence: 99%

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Pathophysiology of hidradenitis suppurativa: a systematic review of the literature

Mendes‐Bastos¹,

Andrade²,

Cabete³

et al. 2022

PJDV

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Hidradenitis suppurative (HS) is a multifactorial, recurrent, chronic inflammatory disease with a significant impact on patient's quality of life. The etiopathogenesis of this complex condition is not fully understood. In this systematic review, we aimed to address and clarify the role of genetics, immunity, endocrinology, and skin microbiome together with risk factors in HS etiopathogenesis. A systematic review, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, was performed using PubMed ® and Web of Science TM databases on December 3rd, 2021, using patient/population, intervention, comparison and outcomes (PICO) criteria, limited to the last 10 years and English. Reports were analyzed by two independent reviewers. A total of 123 reports were included and divided into five sections: genetics, immunity, endocrinology, microbiome, and risk factors. Regarding genetics, up to 30-40% of patients have a positive family history of HS but only a small subset of these harbor genetic variants in components of the gamma-secretase complex. In fact, in more than 90% of HS patients, the genetic features contributing to disease development remain largely unknown. The immune response is also crucial for HS; it is characterized by antimicrobial peptide and proinflammatory cytokine dysregulation, namely interleukin (IL)-IL-23, IL-12, and Th17 immune response. This immune response in local and, consequently, systemic inflammation is amplified in patients with metabolic syndrome. The relationship between metabolic syndrome and HS is clear, and patients with metabolic syndrome have a higher risk of developing HS. The most recent evidence also associates skin microbiota dysbiosis with HS pathogenesis, contributing to local and systemic inflammation. Besides these intrinsic factors, the role of lifestyle in the development of HS is well accepted. Tobacco smoking and obesity are the main risk factors identified as contributing to HS pathogenesis. Chronic inflammation characterizes HS, a debilitating condition with a complex and multifactorial etiopathogenesis. The current model integrates genetics, immunity, endocrinology, and skin microbiome. Notwithstanding, efforts should be made to improve our comprehension of HS etiopathogenesis, hopefully leading to the development of more effective treatments.

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Expert consensus on priority research gaps in dietary and lifestyle factors in hidradenitis suppurativa: a Delphi consensus study

et al. 2023

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Primary alterations during the development of hidradenitis suppurativa

Cited by 25 publications

References 24 publications

Hidradenitis Suppurativa: Absence of Hyperhidrosis but Presence of a Proinflammatory Signature in Patients’ Sweat

Hidradenitis Suppurativa: Absence of Hyperhidrosis but Presence of a Proinflammatory Signature in Patients’ Sweat

Pathophysiology of hidradenitis suppurativa: a systematic review of the literature

Expert consensus on priority research gaps in dietary and lifestyle factors in hidradenitis suppurativa: a Delphi consensus study

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