Synopsis:
Hidradenitis suppurativa is a chronic and frequently debilitating cutaneous disorder that significantly impacts the quality of life of patients. Compared to other cutaneous disorders, such as psoriasis and atopic dermatitis, it is relatively poorly characterized. HS is significantly different from these classic inflammatory skin diseases through the clinical presentation of non-healing skin lesions and the formation of ducts and cysts that become highly inflamed. Our transcriptomic analysis of HS lesions suggests a significant role for innate antimicrobial immunity and altered sweat gland function in HS disease pathology and furthermore revealed a previously unknown set of DEG that overlap with healing wounds.
Recent studies have begun to illuminate the role of sweat gland cells, specifically sweat gland progenitors, in wound healing and re-epithelialization. Sweat glands contain multipotent progenitor cells that can migrate to epidermal layers of the skin and contribute to repair; in addition, eccrine ductal cells participate in re-epithelialization [98, 102]. Sweat glands may also contribute to cutaneous immunity beyond their role in wound repair through production of inflammatory cytokines and DCD, a sweat-gland associated AMP [59, 104]. Therefore, it is possible that sweat glands produce multiple host factors, including antimicrobial DCD that promote epithelial regeneration and that this pathway is dysregulated in HS prohibiting healing of severe HS lesions.
We also uncovered substantial transcriptional overlap between HS lesions and wounded skin, suggesting that HS may represent a wound-like environment. Our analysis could pave the way for development of new therapies for HS. For example, supplementation and activation of natural AMPs, such as DCD, may be promising therapeutic options for the treatment of HS.
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