interleukin-8 and Hidradenitis-Suppurativa

interleukin-8 has been researched along with Hidradenitis-Suppurativa* in 3 studies

Other Studies

3 other study(ies) available for interleukin-8 and Hidradenitis-Suppurativa

ArticleYear
Hidradenitis Suppurativa: Absence of Hyperhidrosis but Presence of a Proinflammatory Signature in Patients' Sweat.
    Acta dermato-venereologica, 2022, Oct-18, Volume: 102

    The role of sweat glands in hidradenitis suppurativa has been largely neglected, despite the fact that its original designation, as "hidrosadénite phlegmoneuse", implied an inflammatory malfunction of the apocrine sweat glands as the underlying pathogenic driver. The aim of this study was to evaluate the role of apocrine sweat glands with respect to the proinflammatory environment of hidradenitis suppurativa. Therefore, gravimetric assessment and multiplex cytokine assays from sweat obtained from patients with hidradenitis suppurativa along with immunofluorescence cytokine/chemokine analysis of lesional apocrine glands- bearing hidradenitis suppurativa skin were performed. Gravimetric assessment of 17 patients with hidradenitis suppurativa revealed that the condition is not associated with hyperhidrosis. However, patients seem to be more affected by subjective sweating. The current data identified a complex proinflammatory signature in hidradenitis suppurativa sweat characterized by a significant upregulation of monocyte chemoattractant protein-1, interleukin-8 (CXCL8), and interferon-γ. In agreement with this, a strong in situ expression of these mediators could be observed in apocrine glands of lesional hidradenitis suppurativa skin. These data shed new light on the proinflammatory capacity of apocrine sweat glands in hidradenitis suppurativa, which may lead to reconsideration of the role of sweat glands in hidradenitis suppurativa pathology.

    Topics: Chemokine CCL2; Hidradenitis Suppurativa; Humans; Hyperhidrosis; Interferon-gamma; Interleukin-8; Sweat; Sweating

2022
The Clinical Significance of Increased Serum Proinflammatory Cytokines, C-Reactive Protein, and Erythrocyte Sedimentation Rate in Patients with Hidradenitis Suppurativa.
    Mediators of inflammation, 2017, Volume: 2017

    To assess inflammatory serum markers including serum proinflammatory cytokines, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) according to the clinical inflammatory activity of patients with hidradenitis suppurativa (HS).. Seventy-four patients with HS were studied based on the Hidradenitis Suppurativa-Physician Global Assessment (HS-PGA) score and Hurley staging system. Proinflammatory cytokines were measured using a multiplex cytokine assay. Twenty-two healthy volunteers were recruited.. Serum interleukin- (IL-) 6, IL-23, soluble tumour necrosis factor alpha (TNF-. Serum proinflammatory cytokines, CRP, and ESR are increased in relation to the clinical inflammatory activity of patients with HS compared with healthy controls. Serum IL-6, CRP, and ESR are effective biomarkers for evaluating the severity of HS.

    Topics: Blood Sedimentation; C-Reactive Protein; Cytokines; Erythrocytes; Hidradenitis Suppurativa; Humans; Interleukin-10; Interleukin-12; Interleukin-1beta; Interleukin-6; Interleukin-8

2017
Immunohistological pointers to a possible role for excessive cathelicidin (LL-37) expression by apocrine sweat glands in the pathogenesis of hidradenitis suppurativa/acne inversa.
    The British journal of dermatology, 2012, Volume: 166, Issue:5

      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

2012