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Cytokine-Mediated Molecular Pathophysiology of Hidradenitis Suppurativa: A Narrative Review
Open accessAbstract
Background: Hidradenitis suppurativa (HS) is a chronic inflammatory condition of the skin that mainly affects the apocrine gland-rich intertriginous areas. The disease manifests as painful nodules, abscesses, and pus-filled tunnels, which can severely impact patient's quality of life. While diagnosis is clinical, successful treatment options for this condition are limited. There has been an increase in research and clinical trials focusing on biomarkers and cytokines for clinical use. Understanding the potential biomarkers and cytokines implicated in HS pathogenesis may allow efficacious and safe treatment options. Summary: A literature review was conducted on nine biomarkers and cytokines. IL-1, IL-10, IL-17, IL-23, TNF-α, YKL-40, G-CSF, NOD2, and the complement system were identified due to their potential clinical utilization and pathophysiological involvement in HS. Key Messages: With further research expanding our understanding of the pathophysiology of HS and the roles these cytokines and biomarkers play, there is potential for utilization as diagnostic markers or development of antagonists against these specific agents for HS management.
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In moderate-to-severe hidradenitis suppurativa, treatment includes targeted biologic agents, notably TNF-α inhibition with adalimumab and IL-17A inhibition with secukinumab, while strategies against the IL-17/IL-23 pathway, IL-1 signaling, and IL-36 and innate immune signaling remain under investigation.
“In moderate-to-severe disease, treatment includes targeted biologic agents, notably TNF-α inhibition with adalimumab, and IL-17A inhibition with secukinumab, while additional therapeutic strategies directed against the IL-17/IL-23 pathway, IL-1 signaling, and IL-36 and innate immune signaling pathways remain under investigation [42,43].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [42]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredHidradenitis suppurativa represents a reprogrammed cutaneous microenvironment in which epithelial dysfunction, immune dysregulation, microbial persistence, and stromal remodeling are tightly integrated.
“Thus, hidradenitis represents a reprogrammed cutaneous microenvironment in which epithelial dysfunction, immune dysregulation, microbial persistence, and stromal remodeling are tightly integrated [40,41,42].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [42]
The Introduction (page unavailable) links hair-follicle dysregulation and immune activation to HS lesions and later scarring; it also mentions bacterial proliferation and *potential* biofilm formation. The Interleukin-17 section describes inflammatory signaling involving keratinocytes, and the Interleukin-1 section describes fibroblast and matrix responses. The review does not establish persistent microbes or show that all four processes are tightly integrated in a reprogrammed cutaneous microenvironment. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn hidradenitis suppurativa, the morphological spectrum is characterized by follicular occlusion, sinus tract formation, and a dense inflammatory infiltrate rich in neutrophils and macrophages.
“In hidradenitis suppurativa, the morphological spectrum is characterized by follicular occlusion, sinus tract formation, and a dense inflammatory infiltrate, rich in neutrophils and macrophages.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [42]
Cytokine profiling in hidradenitis suppurativa reveals involvement of TNF-α, IL-1, and IL-17 pathways, providing a rationale for targeted therapies.
“Cytokine profiling reveals involvement of TNF-α, IL-1, and IL-17 pathways, providing a rationale for targeted therapies.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [42]
In mild hidradenitis suppurativa, treatment relies on topical and systemic anti-inflammatory and antimicrobial therapies, including topical clindamycin and oral tetracyclines or clindamycin-rifampicin, which reduce bacterial load and secondary immune activation.
“In mild disease, treatment relies on topical and systemic anti-inflammatory and antimicrobial therapies, including topical clindamycin and oral tetracyclines or combination regimens such as clindamycin–rifampicin, which help reduce bacterial load and secondary immune activation.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [42]
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Tinca, A. C., Cozac-Szoke, A. R., & Cotoi, O. S. (2026) · Dermatopathology · doi:10.3390/dermatopathology13020022 · Cited by 1
Metadata
- Authors
- Melchor, J., Prajapati, S., Pichardo, R. O., & Feldman, S. R.
- Affiliations
- Wake Forest University Health Sciences (US)
- Corresponding author
- Melchor, Julian
- Venue
- Skin Appendage Disorders
- Publisher
- S. Karger AG
- Published
- 2024
- Volume
- 10
- Issue
- 3
- Pages
- 172-179
- ISSN
- 2296-9160 (ISSN-L)
- 2296-9195
- PMC
- PMC11147516
- OpenAlex
- W4392186016
- Cited by
- 13
- References
- 25
- Citations by year
- 2026: 7 · 2025: 6
- FWCI
- 1.01
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Skin Appendage Disorders (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Florida State University
- Topics
- Health Sciences › Medicine › Dermatology › Hidradenitis Suppurativa and Treatments
- Health Sciences › Medicine › Dermatology › Autoimmune and Inflammatory Disorders
- Health Sciences › Medicine › Rheumatology › Osteomyelitis and Bone Disorders Research
- Keywords
- hidradenitis suppurativa, cytokines, biomarkers, pathogenesis, interleukin-1, IL-10, IL-17, IL-23, TNF-α, YKL-40, granulocyte colony-stimulating factor, NOD2, complement system, apocrine glands, intertrigo, anti-cytokine therapy
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