Recent research published in the Journal of Investigative Dermatology provides new evidence suggesting apocrine glands may play a more significant role in hidradenitis suppurativa than previously thought, challenging decades of conflicting theories about the chronic skin condition's pathogenesis.
While earlier theories suggested apocrine gland inflammation as the primary driver, recent research has focused on follicular obstruction as the central factor. “The literature is fairly divided,” said researcher Amanda M. Nelson from Penn State University College of Medicine. She raised the possibility that “a subset of patients with HS have apocrine gland involvement, whereas others do not.”
Investigators reviewed histological evaluations of axillary apocrine glands from 8 healthy controls and 12 hidradenitis suppurativa (HS) patients, examining lesional and non-lesional skin samples. Apocrine gland size was approximately 50% to 60% smaller in lesional and non-lesional HS skin. Additionally, 50% of apocrine glands from HS patients exhibited degradation—such as intracellular edema, cell lysis, and cell loss—compared to fewer than 10% in healthy controls. The basement membrane zone of apocrine glands in HS skin was also minimally fragmented, contrasting with the intact membranes in healthy controls.
Using single-cell RNA sequencing and immunohistochemistry on samples from three HS patients and three controls, researchers identified decreased expression of cell junction genes and proteins in HS skin glands. These changes may underlie the histologically observed gland damage.
Enhanced signaling pathways were also identified: CXCL16-CXCR6 signaling predominated between apocrine glands and T cells in non-lesional skin, while CXCL1-CXCR2, CXCL8-CXCR2, and serum amyloid A signaling were prominent between gland cells and neutrophils in lesional skin. Immunohistochemistry confirmed the presence of neutrophils and macrophages near apocrine glands, supporting their involvement in inflammatory processes.
Researchers also identified two apocrine gland cell subclusters (AG1 and AG2). AG1 cells were significantly reduced in HS skin and were found to produce neutrophil-recruiting chemokines, highlighting their potential role in immune activation.
Further research could help identify patients with significant apocrine gland involvement and explore potential implications for treatment strategies. The study’s small sample size and variable gland damage across patients are noted limitations.
The authors declared having no competing interests.
