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KMID : 0984920090110020051
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Journal of Skin Barrier Research
2009 Volume.11 No. 2 p.51 ~ p.51
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Skin barrier in acne
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Lee Weon-Ju
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Abstract
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Acne is a chronic inflammatory disorder affecting pilosebaceous units. It is caused by increased sebum secretion, hyperkeratosis of follicular infundibulum, colonization of Propionibacterium acnes, and inflammation. It is characterized by a great variety of clinical lesions. The lesions may be either non-inflammatory or inflammatory. The non-inflammatory lesions are comedones, which may be either open or closed. The inflammatory lesions vary from small papules to pustules to large, tender, fluctuant nodules. Stratum corneum of the skin organizes barrier system to prevent excess water loss, limit percutaneous absorption, and provide protective defense against the natural tendency of microbes to establish and proliferate in the nutrient-rich environment established by the body. The barrier function of stratum corneum is regulated by physical barrier comprising protein-enriched corneocytes and intercellular lipid matrix, and chemical barrier
consisting of antimicrobial peptides and inflammatory cytokines. Disruption of barrier function can provide an explanation for the pathogenesis of a wide variety of common skin diseases, such as psoriasis and atopic dermatitis. There is considerable information on the various factors concerned in barrier function abnormality of acne. The primary change in acne is an alteration in the pattern of keratinization within the pilosebaceous follicle. The disruption of physical barrier in hyperkeratinized follicle is observed in the change of expression of several proteins including involucrin, filaggrin and loricrin. Other charateristic changes in acne include increased sebum secretion and participation of inflammatory cytokines. Increased sebum secretion in hair follicle leads to decrease in the levels of cholesterol, cholesterol ester and linoleic acid, and increase in the amount of fatty acid and squalene. Local deficiency of linoleic acid may relate
to follicular hyperkratinization, and lipoperoxide, mainly due to the peroxidation of squalene, and monounsaturated fatty acid are capable of inducing alteration in keratinocyte proliferation and differentiation. Inflammatory cytokine regulation in acne is important in modulation of pathophysiology and recovery barrier function in response to barrier disruption. Antimicrobial peptides in the skin surface, which may exhibit chemical barrier against bacteria, viruses, or fungi, are constitutionally expressed or effectively induced by inflammatory cytokines, such as interleukin-1 alpha and interleukin-1 beta. Journal review and my research data may provide a novel insight to correlation between pathogenesis and alteration of barrier function in acne.
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KEYWORD
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Skin barrier, Acne, Cytokine, Antimicrobial peptides, Pilosebaceous follicle
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