Inflammation and acne: putting the pieces together.
Acne vulgaris is a common skin disease in which abnormal desquamation, excess sebum production, proliferation of Propionibacterium acnes, and production of proinflammatory mediators all contribute to the pathogenesis of the disease. A review of the literature shows that our current understanding of acne pathogenesis continues to evolve. Recent data suggests that inflammatory mediators may play a more important role than previously realized; however, how these mediators work independently as well as together in acne lesion progression is not well understood. Several cell types and mediators involved in the pathology of acne are responsible for producing or exacerbating an inflammatory response. Here, we present an updated theoretical model of acne lesion progression that highlights the role inflammatory mediators may play throughout acne lesion development.
Alison
A
Harvey
Tu T
TT
Huynh
D000152:Acne Vulgaris / Q000209:etiology* / Q000276:immunology / Q000378:metabolism*; D016207:Cytokines / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008264:Macrophages; D009000:Monocytes; D011425:Propionibacterium acnes / Q000201:enzymology*; D012629:Sebum / Q000378:metabolism; D015398:Signal Transduction; D013601:T-Lymphocytes; D051193:Toll-Like Receptors / Q000378:metabolism
D016207:Cytokines; D051193:Toll-Like Receptors; D019314:Dehydroepiandrosterone Sulfate; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone