From pathogenesis of acne vulgaris to anti-acne agents

Spironolactone-Loaded LeciPlexes as Potential Topical Delivery Systems for Female Acne: In Vitro Appraisal and Ex Vivo Skin Permeability Studies

“…Acne vulgaris is a highly prevalent chronic inflammatory condition of the skin affecting more than 80% of teenagers [1]. Acne peak incidence occurs in 14-17-year-old girls and 16-19-year-old boys [2].…”

“…The pathoetiology of acne is associated with factors that cause changes in the natural skin barrier functions and microorganisms, leading to hyperseborrhea, changed keratinization of the pilosebaceous duct, loss of the skin microbial variety, and inflammation [8]. The main hormones implicated in the etiology of acne include androgens, insulin, and insulin-like growth factor-1 [1,9]. Increased sebum productions stimulates follicular hyperkeratinization, leading to microcomedo [10].…”

Integrated targeted serum metabolomic profile and its association with gender, age, disease severity, and pattern identification in acne

“…Consistent with results for DHEA-S, FFAs were elevated only in female subjects and adolescents, not in the male subjects and adults. Androgens stimulate lipid synthesis [44], and the upregulation of androgens and serum lipids affects acne in female subjects and adolescents. Additional lipidomics data are needed to clarify the lipid mechanism in acne subjects.…”

Acne Protection: Measures & Miseries

“…The main hormones responsible for the development of AV include androgens, insulin and insulin-like growth factor-1. Other factors involved in this process are corticotropin-releasing hormone, α-melanocyte-stimulating hormone and substance P [63]. During puberty, alteration of the sebaceous lipid profile, called dysmenorrhea, stress, irritation, cosmetics and potential dietary factors lead to inflammation and formation of different types of acne lesions [64,65].…”

“…(1) P. acnes is involved in the formation of microcomedones. (2) P. acnes colonization leads to an increase in the cohesiveness of corneocytes during the formation of comedones; (3) in vitro studies have suggested that P. acnes produces lipases, proteases, hyaluronidases, and phosphatases that may cause tissue injury; (4) P. acnes induces the expression of the proinflammatory cytokines IL-8, IL-12, IL-1α, IL-1β, and tumor necrosis factor alpha by innate cells, such as keratinocytes and monocytes, through the TLR2-dependent pathway; (5) host cells have developed a protective antimicrobial response to P. acnes such as antimicrobial lipids, AMPs (human beta-defensin 2, psoriasin and cathelicidin, exhibiting synergistic activities and inducing proinflammatory cytokines/ chemokines via TLR4-and CD14-dependent mechanisms; (6) the peptidoglycan-polysaccharide complexes and lipoteichoic acids of P. acnes stimulate proinflammatory cytokines released from monocytes, demonstrating their high antigenicity in severe acne patients. Increased expression of TLR2 and TLR4 in vivo was found in the epidermal layers of acne lesions for the sensing of peptidoglycans and lipopolysaccharides (LPSs), respectively; (7) P. acnes induces the growth of keratinocytes in vitro and upregulates the production of proinflammatory cytokines via a heat-shock GroEL protein; (8) MMPs, produced by different types of cells, including keratinocytes and sebocytes, play important roles in acne inflammation, dermal matrix destruction and hyperproliferative skin disorders.…”