Keratin expression in pilosebaceous epithelia in truncal skin of acne patients

Hughes, B.R.; Morris, C J; Cunliffe, W. J.; Leigh, Irene M.

doi:10.1111/j.1365-2133.1996.tb07609.x

Cited by 81 publications

(61 citation statements)

References 47 publications

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“…Similarly, suprabasal immunolabelling of keratin 16 (K16), a phenotypic marker of hyperproliferating and abnormally differentiating keratinocytes, is found in ductal keratinocytes of acne lesions (fig. 2) [8]. These data are further supported by the finding, using in situ hybridization, that transcripts of K6, the expression partner of K16, are also found suprabasally in the follicle wall of microcomedones and comedones but not in control follicles [9].…”

Section: Aetiology Of Comedogenesissupporting

confidence: 73%

Comedogenesis: Some Aetiological, Clinical and Therapeutic Strategies

et al. 2003

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Hypercornification is an early feature of acne and usually precedes inflammation. It is associated with ductal hyperproliferation, and there are many controlling factors such as androgens, retinoids, sebum composition and cytokines. Cycling of normal follicles and of comedones may explain the natural resolution of comedones and, in the longer term, resolution of the disease itself. There is a need to tailor treatment according to comedonal type. Suboptimal therapy can often result from inappropriate assessments of comedones, especially microcomedones, sandpaper comedones, submarine comedones and macrocomedones. Macrocomedones can produce devastating acne flares, particularly if patients are inappropriately prescribed oral isotretinoin. Gentle cautery under topical local anaesthesia is a useful therapy in the treatment of such lesions. The newer retinoids and new formulations of all-trans-retinoic acid show a better benefit/risk ratio.

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Section: Aetiology Of Comedogenesissupporting

confidence: 73%

Comedogenesis: Some Aetiological, Clinical and Therapeutic Strategies

et al. 2003

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“…154 In comparison to controls, acne patients exhibited an increased filaggrin expression. 155 In the comedone wall an increased suprabasal expression of K6 and K16, and panepithelial expression of K17 could be demonstrated. 155 It is noteworthy that the expression of FGFR2b, IL1 receptor type I and of keratins K6, K16 and K17 co-localize in suprabasal cells pointing to their close spatial and functional relations for the induction of activated keratinocytes.…”

Section: Ser252trp-fgfr2-mutation and Comedogenesismentioning

confidence: 94%

“…155 In the comedone wall an increased suprabasal expression of K6 and K16, and panepithelial expression of K17 could be demonstrated. 155 It is noteworthy that the expression of FGFR2b, IL1 receptor type I and of keratins K6, K16 and K17 co-localize in suprabasal cells pointing to their close spatial and functional relations for the induction of activated keratinocytes. 35,[156][157][158] Aberrant α 2 -and α 3 -integrin expression around comedones and uninvolved pilosebaceous follicles from acne patients further support the activated keratinocyte status of follicular keratinocytes in acne vulgaris.…”

Section: Ser252trp-fgfr2-mutation and Comedogenesismentioning

confidence: 94%

“…154 Increased expression of K17 could be detected in sebaceous glands and sebaceous ducts of uninvolved skin of acne patients, although sebaceous glands showed heterogeneity in keratin expression, with some lobules expressing keratins K1, K5, K7, K10, K14 and K17. 155 Inhibiton of the ectopeptidases dipeptidyl peptidase IV and aminopeptidase N on human sebocytes induced IL-1ra and slightly decreased total neutral lipid production, suppressed proliferation of sebocytes and enhanced terminal differentiation. 168 Furthermore, ectopetidase inhibitors suppressed proliferation and IL-2 production of Propionibacterium acnes-stimulated T-cells ex vivo and enhanced the expression of transforming growth factor-β 1 (TGFβ 1 ).…”

Section: Interleukin-1α and Sebocyte Activationmentioning

confidence: 99%

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Role of FGFR2-signaling in the pathogenesis of acne

Melnik

2009

Dermato-Endocrinology

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It is the purpose of this review to extend our understanding of the fibroblast growth factor (FGF) receptor-2b-signaling network in the pathogenesis of acne. A new concept of the role of FGFR2b-signaling in dermal-epithelial interaction for skin appendage formation, pilosebaceous follicle homeostasis, comedogenesis, sebaceous gland proliferation and lipogenesis is presented. The FGFR2-gain-of-function mutations in Apert syndrome and unilateral acneiform nevus are most helpful model diseases pointing the way to androgen-dependent dermalepithelial FGFR2-signaling in acne. Androgen-mediated upregulation of FGFR2b-signaling in acne-prone skin appears to be involved in the pathogenesis of acne vulgaris. In organotypic skin cultures, keratinocyte-derived interleukin-1α stimulated fibroblasts to secrete FGF7 which stimulated FGFR2b-mediated keratinocyte proliferation. Postnatal deletion of FGFR2b in mice resulted in severe sebaceous gland atrophy. The importance of FGFR2b in sebaceous gland physiology is further supported by the mode of action of anti-acne agents which have been proposed to attenuate FGFR2b-signaling. Downregulation of FGFR2b-signaling by isotretinoin explains its therapeutic effect in acne. Downregulation of FGFR2b-signaling during the first trimester of pregnancy disturbs branched morphogenesis and explains retinoid embryotoxicity. Insulin-like growth factor-1 (IGF-1), the mediator of growth hormone during puberty, intracts with androgen-dependent FGFR2b-signaling and links androgen-and FGF-mediated signal transduction important in sebaceous gland homeostasis. The search for a follicular defect in the dermalepithelial regulation of growth factor-signaling in acne-prone skin appears to be a most promising approach to clarify the pathogenesis of acne.

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“…The hyperproliferation of ductal keratinocytes has been confirmed by immunohistochemical staining with monoclonal antibody Ki-67, by an increase in 3 H-thymidine labeling of comedones and the presence of keratins 6 and 16 [5, 6, 7]. The mechanism by which this process occurs is not elucidated.…”

Section: Abnormal Ductal Keratinizationmentioning

confidence: 99%

The Role of Innate Immunity in the Pathogenesis of Acne

et al. 2003

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Acne is a multifactorial disease of the pilosebaceous follicle. The most significant pathogenetic factors of acne are: abnormal ductal keratinization, increased sebum secretion, abnormalities of the microbial flora and inflammation. The pilosebaceous unit is an immunocompetent organ. Keratinocytes and sebocytes may act as immune cells capable of pathogen recognition and abnormal lipid presentation, and they might have an important role in initiating and perpetuating the activation of both innate and adaptive immune responses. The elements of the skin immune system are involved in the development of both noninflammatory and inflammatory acne lesions.

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Keratin expression in pilosebaceous epithelia in truncal skin of acne patients

Cited by 81 publications

References 47 publications

Comedogenesis: Some Aetiological, Clinical and Therapeutic Strategies

Comedogenesis: Some Aetiological, Clinical and Therapeutic Strategies

Role of FGFR2-signaling in the pathogenesis of acne

The Role of Innate Immunity in the Pathogenesis of Acne

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