# A Novel Epidermis Model Using Primary Hidradenitis Suppurativa Keratinocytes

## TL;DR

Researchers created a new lab-grown epidermis model using skin cells from hidradenitis suppurativa patients to study the disease and test treatments.

## Contribution

A novel in vitro epidermis model using primary HS keratinocytes was developed for studying HS pathology and treatment.

## Key findings

- The HS-epidermis model showed the expected differentiation pattern through immunohistochemical staining.
- The model secreted inflammatory cytokines interleukin-1β and TNF-α, reflecting HS inflammation.
- The model could be used to study biomarkers and barrier function for new topical treatments.

## Abstract

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease. Patients can present with inflammatory nodules, abscesses up to fistulas, or sinus tracts in intertriginous body parts. Occlusion of the sebaceous gland unit leads to its rupture, with a subsequent exuberant immune response. Given there is still no causative therapy, to better understand HS and develop novel therapeutic concepts, research activities in the HS field are constantly growing. Primary skin cells, blood cells, and ex vivo explant cultures from HS patients have been previously used as HS cell culture models. In vitro reconstituted epidermal models are established to study inflammatory dermatoses, such as psoriasis or atopic dermatitis. For HS, the exploration of epidermis models would be an excellent addition, e.g., biomarkers or barrier function in testing new topic treatment options. We therefore established a stratified in vitro HS epidermis model based on primary cells from HS lesions. After isolating keratinocytes from lesional skin, we cultured them submerged in a transwell system. To induce differentiation, we then lifted them to the air-liquid interface. Immunohistochemical staining demonstrated that our HS-epidermis model meets the expected differentiation pattern. In addition, we detected the secretion of the inflammatory cytokines interleukin-1β and TNF-α.