title: Hidradenitis suppurativa: the role of deficient cutaneous innate immunity.
abstract: OBJECTIVE
  To evaluate the expression of innate immunity markers at the site of nodules caused by hidradenitis suppurativa (HS).
  
  
  METHODS
  Prospective analysis of 12 patients with HS.
  
  
  METHODS
  Unité de Cancéro-Dermatologie, Nantes Hospital, Nantes; Service de Dermatologie, Poitiers Hospital, Poitiers; and Service de Dermatologie, Clinique de Courlancy, Reims, France
  
  
  METHODS
  Twelve patients (Hurley stage I or II) in whom the disease had progressed for at least 6 months and who had a minimum of 2 closed nodules in typical sites.
  
  
  METHODS
  Two biopsies were performed at baseline: one in a closed inflammatory nodule and one in healthy adjoining skin. Patients were treated for 3 months with zinc gluconate at a dosage of 90 mg/d. A new biopsy was then performed in the same nodule. Innate immunity markers (toll-like receptors 2, 3, 4, 7, and 9; intercellular adhesion molecule 1; interleukin [IL] 6 and 10; tumor necrosis factor; α melanocyte stimulating hormone; transforming growth factor β; β-defensin 2 and 4; and insulinlike growth factor 1) were studied by immunohistochemical analysis.
  
  
  RESULTS
  We observed significantly decreased expression (P < .001) of all the innate immunity markers studied except IL-10 in nonlesional and lesional HS skin. The downregulation of innate markers was significantly stronger in lesional HS skin compared with normal skin except for tumor necrosis factor. Three months of zinc treatment induced a significant increase in the expression of all the markers involved in innate immunity.
  
  
  CONCLUSIONS
  Our study demonstrates for the first time, to our knowledge, that a deficiency of the main innate immunity markers in typical HS sites may explain the development of chronic inflammatory nodules in this disease.
authors: Institut National de la Santéet de la Recherche Medicale (INSERM), U892, Centre de Recherche en Cancérologie Nantes-Angers, France. brigitte.dreno@wanadoo.fr
authors: Brigitte
authors: B
authors: Dréno
authors: Amir
authors: A
authors: Khammari
authors: Anabelle
authors: A
authors: Brocard
authors: Dominique
authors: D
authors: Moyse
authors: Eric
authors: E
authors: Blouin
authors: Gerard
authors: G
authors: Guillet
authors: Fabienne
authors: F
authors: Léonard
authors: Anne-Chantal
authors: AC
authors: Knol
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D005260:Female; D005942:Gluconates / Q000494:pharmacology* / Q000627:therapeutic use; D017497:Hidradenitis Suppurativa / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D011446:Prospective Studies; D012867:Skin / Q000276:immunology*; D018709:Statistics, Nonparametric; D051193:Toll-Like Receptors / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult; D000521:alpha-MSH / Q000378:metabolism; D023083:beta-Defensins / Q000378:metabolism
chemical_list: D015415:Biomarkers; C106641:DEFB4A protein, human; D005942:Gluconates; D015850:Interleukin-6; D051193:Toll-Like Receptors; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D023083:beta-Defensins; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10; D000521:alpha-MSH; D007334:Insulin-Like Growth Factor I; C030691:gluconic acid