muramidase and Hidradenitis-Suppurativa

Hidradenitis suppurativa (HS) is a chronic inflammatory and debilitating disease of the skin. No biomarkers for this disease exist.. We set out to test whether angiotensin-converting enzyme (ACE), lysozyme, soluble interleukin 2 receptor (sIL-2R) and S100A8/A9 (calprotectin) are elevated in patients with HS.. Serum was collected from 29 patients with HS at different stages of the disease, and from 51 controls. ACE, lysozyme, sIL-2R and S100A8/A9 levels were measured. Clinical observation of disease activity was scored according to the Hurley grading system and by a physician global score (PGS) of disease severity.. Serum levels of lysozyme and ACE were not increased above the normal reference values in controls or patients with HS. Levels of sIL-2R and S100A8/A9 were significantly higher in patients with HS than in controls (P<0·001 for both sIL-2R and S100A8/A9). Based on the receiver operating characteristic curves, the optimum sIL-2R and S100A8/A9 cut-off values were 375 U mL(-1) and 680 ng mL(-1), respectively, with a sensitivity of 0·79 and specificity of 0·78 for sIL-2R, and 0·86 and 0·88, respectively, for S100A8/A9. No correlations with Hurley classification scores were found. However, when using PGS of disease activity to categorize patients, levels of S100A8/A9, but not sIL-2R, tended to be higher in patients with more active disease.. Levels of S100A8/A9 and sIL-2R, but not ACE or lysozyme, are elevated in the serum of patients with HS. However, there is no correlation between S100A8/A9 or sIL-2R levels and disease stage according to the Hurley classification system. Further research is needed to study the potential of S100A8/A9 to score disease activity in larger cohorts of patients and to predict disease flares.

Topics: Adult; Aged; Biomarkers; Calgranulin A; Calgranulin B; Case-Control Studies; Female; Hidradenitis Suppurativa; Humans; Lymphocytes; Male; Middle Aged; Muramidase; Myeloid Cells; Peptidyl-Dipeptidase A; Receptors, Interleukin-2; ROC Curve; Young Adult

  The cause of follicular occlusion, a key early event in the pathogenesis of hidradenitis suppurativa (HS), also known as acne inversa, remains unknown.. To identify changes, if any, in the antimicrobial peptide (AMP) and cytokine expression profile of HS affected human skin.. 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 (n = 12). The lesional skin from patients with HS was histologically subclassified based on the predominance of inflammation vs. scarring.. 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..   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.

Topics: Adult; alpha-MSH; Antimicrobial Cationic Peptides; beta-Defensins; Case-Control Studies; Cathelicidins; Chemotactic Factors; Dermis; Epidermis; Female; Hidradenitis Suppurativa; Humans; Immunohistochemistry; Interleukin-8; Male; Middle Aged; Muramidase; S100 Calcium Binding Protein A7; S100 Proteins; Sweat Glands; Tumor Necrosis Factor-alpha; Up-Regulation; Young Adult