The skin serves not only as a physical barrier but also as a dynamic immune interface, maintained through constant interactions with environmental stimuli. Central to this function is the bidirectional communication between the peripheral nervous system (PNS) and cutaneous immune cells, which together regulate homeostasis, wound healing, and pathogen defense. Disruption of this neuro-immune crosstalk may underlie the pathology of inflammatory skin diseases such as hidradenitis suppurativa (HS).
HS is a chronic, debilitating condition affecting up to 4% of the European population, characterised by painful nodules, abscesses, and sinus tracts in apocrine-rich regions. While disease onset is linked to follicular structures, current evidence fails to explain its chronicity. Chronic immune dysregulation seems to be central to pathogenesis, although its precise anatomical localisation remains unclear. Current therapies targeting TNF-α and IL-17 pathways provide symptomatic relief but do not fully resolve disease mechanisms.
This project aims to investigate the role of cutaneous innervation in HS. Clinical skin biopsies (lesional, perilesional, and uninvolved) will be collected across Hurley stages I–III. Samples will undergo paraffin-embedding, antigen retrieval, and immunohistochemical (IHC) staining. High-resolution confocal microscopy, supported by Incucyte® Neurotrack Analysis, will assess neuronal morphology including neurite length, branching, dendritic swelling, and epidermal penetration. Transmission electron microscopy (TEM) will further characterise fine structural interactions between small fibre endings and Schwann cells where time allows.
I hypothesise that HS skin exhibits altered innervation patterns and neuro-immune interactions, contributing to persistent inflammation. By elucidating the role of the PNS in HS pathogenesis, this research may provide novel insights into the anatomical specificity and chronic nature of disease presentation, informing future therapeutic strategies.