Hidradenitis suppurativa - The role of interleukin-17, the aryl hydrocarbon receptor and the link to a possible fungal aetiology

Hidradenitis Suppurativa (HS) is a chronic, recurrent, debilitating skin disease of the hair follicle that usually presents after puberty with painful, deep-seated, inflamed lesions in the apocrine gland bearing areas of the body, most commonly the axillae, inguinal and anogenital regions. The pathophysiology of the disease remains elusive, with newer therapies targeting various aspects of the dysregulated immune system. This presents a useful opportunity to look at the cytokine profile in HS and other inflammatory conditions that share similar patterns with the aim of teasing out less considered explanations for HS pathogenesis. It has been observed that IL-17 appears to be the most common denominator linking HS with other immune mediated diseases like Crohn, ulcerative colitis, multiple sclerosis and psoriasis. Given that IL-17 plays an important role in antifungal immunity, evidenced by the cytokine pattern in fungal disease and the bulk of data citing their potential involvement in Crohn, ulcerative colitis, multiple sclerosis and psoriasis; it is fair to suggest the need to explore the role that fungi play in the setting of HS going forward. The aryl hydrocarbon receptor (ahr) is a ubiquitous and largely conserved entity that is gaining interest in inflammatory conditions such as psoriasis and atopic dermatitis. It is well known to modulate autoimmune states. Its activation by both exogenous and endogenous agents result in secretion of IL-17 by Th17 cells. One of such agents is the tryptophan metabolite 6-formylindolo [3,2-b] carbazole (FICZ)-which can be produced by microorganisms such as fungi. It will be interesting to explore its usefulness in HS pathogenesis.

Automated summary

HS is a chronic, recurrent skin disease with complex pathophysiology possibly related to immune system dysregulation, and IL-17 may be a common factor linking HS with other immune-mediated diseases. Further exploration into the role of fungi and aryl hydrocarbon receptor in HS pathogenesis is needed.