Get access

Immunohistological pointers to a possible role for excessive cathelicidin (LL-37) expression by apocrine sweat glands in the pathogenesis of hidradenitis suppurativa/acne inversa

Authors


  • Current affiliation: Department of Dermatology, Boston University School of Medicine, 609 Albany Street, Boston, MA, 02118, U.S.A.

  • Funding sources
    This study was supported in part by DFG Centre of Excellence, ‘Inflammation at Interfaces’. E.A.L. is supported by a Medical Research Council Clinical Research Training Fellowship.

  • Conflicts of interest
    None declared.

  • F.G.B, R.G., E.A.L. and W.M.T. contributed equally to this work.

Vladimir U. Emelianov
E-mail: vemelianov@mail.ru

Abstract

Summary Background  The cause of follicular occlusion, a key early event in the pathogenesis of hidradenitis suppurativa (HS), also known as acne inversa, remains unknown.

Objectives  To identify changes, if any, in the antimicrobial peptide (AMP) and cytokine expression profile of HS affected human skin.

Methods  Quantitative immunohistomorphometry was used to compare the in situ protein expression of selected AMPs and cytokines in lesional HS skin from 18 patients with that in healthy skin (= 12). The lesional skin from patients with HS was histologically subclassified based on the predominance of inflammation vs. scarring.

Results  Compared with healthy controls, significantly increased immunoreactivity for cathelicidin (LL-37) was noted in the apocrine sweat gland and distal outer root sheath (ORS) of the hair follicle (HF) epithelium in lesional HS skin. Immunoreactivity for LL-37, psoriasin, human β-defensin 3 (hBD3), α-melanocyte stimulating hormone (α-MSH), macrophage migration inhibitory factor (MIF), tumour necrosis factor (TNF)-α and interleukin (IL)-8 was significantly increased in HS epidermis. LL-37 and TNF-α immunoreactivity was also increased in the dermis of lesional HS skin. In contrast, lysozyme expression was decreased in the epidermis of lesional HS skin, while that of TNF-α and IL-8 was decreased in the proximal ORS of HFs in HS lesions. These differences were most pronounced in HS with predominant inflammation.

Conclusions  Our observations raise the question as to whether excessive secretion of AMPs by the skin, in particular by the apocrine sweat glands, distal HF epithelium, and epidermis, may attract inflammation and thus facilitate or promote HS development.

Ancillary