The critical role of macrophages in the pathogenesis of hidradenitis suppurativa

Hidradenitis suppurativa Research

Author(s): Shah A, Alhusayen R, Amini-Nik S

INTRODUCTION: Hidradenitis suppurativa (HS) is a painful chronic inflammatory disease with a prevalence between 1 and 4% of general population. The pathogenesis of HS long eluded scientists, but growing evidence suggests that it is a consequence of inflammatory dysregulation.

FINDINGS: Recent studies suggest that dysregulated immune response to skin flora and overexpression of inflammatory cytokines leads to chronic skin inflammation seen in HS. Macrophages are the most numerous inflammatory cells found in HS infiltrates and release numerous pro-inflammatory cytokines such as IL-23, and IL-1β and TNF-α, exacerbating the inflammation and contributing to the pathogenesis of HS. Furthermore, in HS, there is dysregulated function of other immune players closely associated with macrophage function including: matrix metalloproteases (MMP) 2 and 9 overexpression, toll-like receptor upregulation, impaired Notch signalling, NLRP3 inflammasome upregulation, and dysregulated keratinocyte function. Lifestyle factors including obesity and smoking also contribute to macrophage dysfunction and correlate with HS incidence.

CONCLUSIONS: The overexpression of pro-inflammatory cytokines and subsequent efficacy of anti-cytokine biologic therapies highlights the importance of managing macrophage dysfunction. Future therapies should target key molecular drivers of macrophage dysfunction such as TLR2 and NLRP3 overexpression.

Dermatology Journal and/or Publisher

Journal Name: Inflammation research : official journal of the European Histamine Research Society … [et al.]
Journal Abbreviation: Inflamm. Res.
Journal Date Published:

National Center for Biotechnology Information

PMID: 28656364
Article Source:
Lasted Revision: 2017-11-17

Abstract Source: National Center for Biotechnology Information, U.S. National Library of Medicine Abstract Query for Hidradenitis suppurativa (HS).


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