Active Hidradenitis Suppurativa lesions are associated with elevated Interferon-Gamma (IFN-γ) in wound exudate

November 10, 2016

A study by The George Washington University Ideas to Health laboratory indicates that the pro-inflammatory cytokine Interferon-gamma (IFN-γ) was significantly elevated in wound fluid exudate from HS patients. This finding lends support to the hypothesis that immune mechanisms play a role in the pathogenesis of HS and suggests that IFN-γ may play a crucial role as a molecular driver in HS disease activity. Future studies in the Ideas to Health Laboratory are focused on identifying biomarkers of disease activity in HS and investigating proinflammatory pathways that might help identify treatment options for this challenging disease.

Purpose of the study

Hidradenitis suppurativa (HS) is a disabling, chronic, recurrent inflammatory disease of the apocrine sweat glands. It affects 1% to 4% of adults, and is more common in young, African American women. There is currently no known cure, and the mechanisms driving the disease are unknown. There is an unmet need to understand the molecular drivers of HS in order to develop new treatments and improve clinical outcomes for patients. The purpose of this study was to investigate inflammatory cytokines in effluent from HS lesions and to identify potential local drivers of inflammation in HS.

How was this study done?

Wound fluid specimens from 8 HS patients and 8 age-matched chronic wound patients were selected for analysis. The Hidradenitis Suppurativa Score (HSS) was used to determine extent of HS activity. Cytokine analysis was conducted using Meso Scale Discovery cytokine and proinflammatory panels.

What were the major findings?

Interferon-gamma (IFN-γ) was significantly elevated in the HS effluent compared to chronic wounds. HS effluent also had higher levels of TNF-β. There was no significant difference in any other cytokines. There was no significant difference in demographics in the HS compared to chronic wound cohorts.

What is the impact of this work?

The immune system related defects in disease HS are not well understood and mechanisms driving disease activity are not known. This study not only confirms that cytokine profiles can be reliably measured on HS lesion effluent, but also suggests that IFN- γ likely contributes to the local inflammatory response in HS and may be crucial molecular driver of tissue injury in HS.

This research was supported by:

Study supported by award R01NR013888 from the National Institute of Nursing Research and by award number UL1 TR000075 from the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through the Clinical and Translational Science Awards Program (CTSA).  

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