Hidradenitis suppurativa (HS) is a chronic, recurrent inflammatory skin disorder of the pilosebaceous unit, characterized by nodules, abscesses, and sinus tracts formation in apocrine gland-bearing skin. Increasing evidence suggests that HS is not solely a localized dermatological condition, but part of a broader systemic inflammatory state closely associated with metabolic dysfunction. Meta-inflammation, defined as a chronic, low-grade inflammatory response driven by metabolic imbalance, has emerged as a key mechanism linking obesity, insulin resistance, and immune dysregulation to the pathogenesis and progression of HS. It has indeed been demonstrated in numerous studies that HS and metabolic syndrome (MetS) share a core link through meta-inflammation, driven by common pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. These pathways, along with insulin resistance and obesity-related adipose tissue dysfunction, drive both skin disease severity and metabolic comorbidities often creating a self-perpetuating cycle of inflammation and tissue damage. Understanding the interplay between meta-inflammation and HS provides important insights into disease heterogeneity and highlights the need for a multidisciplinary therapeutic approach. Targeting meta-inflammation through lifestyle interventions, weight management, and immuno-metabolic therapies may complement established treatments and improve clinical outcomes. In this review, we explore the pathogenic link between meta-inflammation and HS and discuss the therapeutic targets arising from this intricate interplay.
Meta-inflammation in Hidradenitis suppurativa: from pathogenic evidence to therapeutic approaches / C. Moltrasio, A.K.. - In: FRONTIERS IN IMMUNOLOGY. - ISSN 1664-3224. - 17:(2026 May 25), pp. 1827227.1-1827227.10. [10.3389/fimmu.2026.1827227]
Meta-inflammation in Hidradenitis suppurativa: from pathogenic evidence to therapeutic approaches
A.V. Marzano
Co-ultimo
2026
Abstract
Hidradenitis suppurativa (HS) is a chronic, recurrent inflammatory skin disorder of the pilosebaceous unit, characterized by nodules, abscesses, and sinus tracts formation in apocrine gland-bearing skin. Increasing evidence suggests that HS is not solely a localized dermatological condition, but part of a broader systemic inflammatory state closely associated with metabolic dysfunction. Meta-inflammation, defined as a chronic, low-grade inflammatory response driven by metabolic imbalance, has emerged as a key mechanism linking obesity, insulin resistance, and immune dysregulation to the pathogenesis and progression of HS. It has indeed been demonstrated in numerous studies that HS and metabolic syndrome (MetS) share a core link through meta-inflammation, driven by common pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. These pathways, along with insulin resistance and obesity-related adipose tissue dysfunction, drive both skin disease severity and metabolic comorbidities often creating a self-perpetuating cycle of inflammation and tissue damage. Understanding the interplay between meta-inflammation and HS provides important insights into disease heterogeneity and highlights the need for a multidisciplinary therapeutic approach. Targeting meta-inflammation through lifestyle interventions, weight management, and immuno-metabolic therapies may complement established treatments and improve clinical outcomes. In this review, we explore the pathogenic link between meta-inflammation and HS and discuss the therapeutic targets arising from this intricate interplay.| File | Dimensione | Formato | |
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