The antimicrobial peptide dermcidin—normally found in human sweat—may play a role in the pathogenesis of hidradenitis suppurativa (HS), report researchers from the George Washington University School of Medicine & Health Sciences in Washington, D.C.
In a press release from the university released on Apr. 25, 2019, Dr. Victoria Shanmugam, an associate professor of medicine at the school who led the research, said: “Until now, the molecular drivers of HS have been poorly understood.”
“Traditional therapies have thus far been disappointing. However, TNF-α inhibitors like infliximab and adalimumab have shown efficacy.”
In a study published online ahead of print in Clinical and Experimental Dermatology (Mar. 3, 2019), Dr. Shanmugam and her team measured mRNA expression in 10 skin samples from patients with HS and 11 skin specimens from patients who underwent abdominoplasty, as controls.
They found that both dermcidin and the cytokine regulator interleukin (IL)‐37 were both significantly downregulated in the HS specimens.
“These findings suggest regulators of the innate immune response and particularly antimicrobial peptide production may play a role in HS pathogenesis,” Dr. Shanmugam said.
The data also suggests multiple biological pathways are disrupted in HS, indicating that inflammatory pathways merit additional investigation as potential drivers of the disease. Further analysis showed that the interferon‐signalling pathway, leucocyte extravasation pathway, T helper 1 and 2 pathways and nuclear factor of activated T cells were the five most up-regulated pathways in the HS samples.
Further study is needed, said Dr. Shanmugam, in order to fully understand the role of antimicrobial peptides, particularly dermcidin, in the pathogenesis of HS and whether these pathways lend themselves to the development of new therapeutic options for the disease.