J. L. Roberson1,2, S. Nisar1,3, B. C. Carney1,4, A. Alkhalil1, L. T. Moffatt1,4, J. W. Shupp1,3,4,5 1MedStar Health Research Institute,Firefighters’ Burn And Surgical Research Laboratory,Washington, DC, USA 2George Washington University School Of Medicine And Health Sciences,Department Of Surgery,Washington, DC, USA 3Washington Hospital Center,The Burn Center, Department Of Surgery,Washington, DC, USA 4Georgetown University Medical Center,Department Of Biochemistry And Molecular And Cellular Biology,Washington, DC, USA 5Georgetown University Medical Center,Department Of Surgery,Washington, DC, USA
Introduction:
Hidradenitis Suppurativa (HS) is a chronic inflammatory skin condition that presents as painful, draining abscesses which undergo repeated cycles of inflammation and healing with fibrosis. Hurley stage I is characterized by isolated nodules, stage II with recurrent inflammation and tract formation, and stage III involves coalesced tracts. At the present time, there is no definitive medical treatment for HS and a great deal of patients eventually undergo surgical resection. This study aims to evaluate the cytoarchitecture and cell surface markers present in HS patients to further understand the disease and identify potential therapeutic targets that may be used to stop HS progression, ultimately providing an alternative to surgery.
Methods:
Samples for cytoarchitecture analysis were formalin-fixed, paraffin embedded skin biopsies from 11 patients with HS who underwent surgical excision between May 2014 to June 2018. Six patients had stage III disease, one was stage I, and the rest were not staged. Histopathologic analysis included Hematoxylin and Eosin (H&E) staining and imaging at 10x magnification. These were compared with healthy human skin cytoarchitecture, analyzed as above, side-by-side.
Anti-CD3, a T-cell marker, and anti-CD31, a PECAM and vascular T-cell specific marker, were used for immunohistochemical (IHC) analysis. IHC was conducted in four HS and four healthy skin specimens with six regions of interest (three epidermal and three dermal) per sample. Cellular quantification was performed at 40x magnification and compared with Student’s t-test.
Results:
Histopathologic examination showed that HS skin had a wider epidermal layer, extending into and engulfing the dermis, leaving intact dermal islands. Collagen fibers were disorganized compared with healthy skin. Other histological differences included formation of an epithelialized tract within the dermis and epithelialization around a hair follicle. Neither apocrine, eccrine nor sebaceous gland histology was noted to be different between normal and HS skin.
Furthermore, there was extensive cellular infiltration and aggregation in the dermis of 10 out of 11 HS patients. IHC analysis revealed that, at the dermal level, HS lesions had a significantly greater quantity of CD3+ (324.29±139.28 vs. 14.93±16.32, p<0.0001), and CD31+ (322.15±155.46 vs. 2.84±5.56, p<0.0001) cells/mm2 than healthy skin samples.
Conclusion:
Epidermal and dermal cytoarchitecture of HS lesions differ in comparison to healthy skin. Furthermore, HS lesions demonstrate a significantly greater dermal lymphocytic infiltrate compared to healthy skin. Given that these samples are architecturally and cellularly consistent with HS, transcriptomic and immunohistochemical analysis for genes and proteins of interest are ongoing, with the goal of identifying potential non-surgical therapeutic targets.