Study: Intrinsic Defect Leads to Inflammation in HS

The chronic, inflammatory, debilitating, follicular skin disease hidradenitis suppurativa (HS) has a high prevalence in the general population. However the physiopathology of the condition is still poorly understood.

The use of antibiotics and immunosuppressive agents for therapy suggest a deregulated immune response to microflora, according to a recent study, which was published in The Journal of Investigative Dermatology.
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For the study, the researchers used cellular and gene expression analyses and found an increased number of infiltrating CD4+ T cells secreting interleukin-17 (IL-17) and interferon-γ (IFNγ) in perilesional and lesional skin of HS patients. They noted that IL-22 secreting CD4+ T cells are not enriched in HS lesions contrasting with increased number of those cells in HS patients’ blood.

The study demonstrated that keratinocytes isolated from hair follicles of HS patients secreted significantly more IL-1β, IP-10 and CCL5 (RANTES), either constitutively or upon patterns recognition receptors (PRR) stimulations. In addition, they displayed a distinct pattern of antimicrobial peptides (AMPs) production.

“These findings point out a functional defect of keratinocytes in HS leading to a balance prone to inflammatory responses. This is likely to favor a permissive environment for bacterial infections and chronic inflammation characterizing clinical outcomes in HS patients,” the researchers concluded.

Reference:
Hotz C, Boniotto M, Guguin A, Surenaud M, Jean-Louis F, Tisserand P et al. Intrinsic defect in keratinocyte function leads to inflammation in Hidradenitis suppurativa [published online May 17, 2016]. J Invest Dermatol. doi: 10.1016/j.jid.2016.04.036.