epidermal-growth-factor and Dermatitis

Topical application of epidermal growth factor (EGF) promotes wound healing and may reduce the risk of laser-induced postinflammatory hyperpigmentation (PIH).. To investigate the effect of an EGF-containing cream on the incidence of laser-induced PIH.. Twenty-five Korean patients with senile lentigines were recruited and underwent 532-nm Q-switched Nd:YAG laser treatment. Postoperatively, patients applied either an EGF-containing cream or a control cream to the laser-treated area. Skin color and transepidermal water loss (TEWL) were measured on Days 0, 3, 7, and 35 using a Mexameter and Tewameter, respectively.. The EGF-containing cream resulted in a nonsignificant reduction in the laser-induced increase in TEWL (p = .052 on Day 7) but significantly decreased the melanin index and incidence of PIH on Day 35 (p = .031 and p = .027, respectively).. Epidermal growth factor-containing creams may be an effective measure to prevent laser treatment-induced PIH in Asian patients.

Topics: Adult; Aged; Dermatitis; Dermatologic Agents; Epidermal Growth Factor; Erythema; Female; Humans; Hyperpigmentation; Lasers, Solid-State; Lentigo; Male; Middle Aged; Skin Cream; Water Loss, Insensible

Epidermal growth factor (EGF) family members, including epiregulin (EP), play a fundamental role in epithelial tissues; however, their roles in immune responses and the physiological role of EP remain to be elucidated. The skin has a versatile system of immune surveillance. Biologically active IL-1alpha is released to extracellular space upon damage from keratinocytes and is a major player in skin inflammation. Here, we show that EP is expressed not only in keratinocytes but also in tissue-resident macrophages, and that EP-deficient (EP(-/-)) mice develop chronic dermatitis. Wound healing in the skin in EP(-/-) mice was not impaired in vivo, nor was the growth rate of keratinocytes from EP(-/-) mice different from that of WT mice in vitro. Of interest is that in WT keratinocytes, both IL-1alpha and the secreted form of EP induced down-regulation of IL-18 mRNA expression, which overexpression in the epidermis was reported to induce skin inflammation in mice, whereas the down-regulation of IL-18 induced by IL-1alpha was impaired in EP(-/-) keratinocytes. Although bone marrow transfer experiments indicated that EP deficiency in non-bone-marrow-derived cells is essential for the development of dermatitis, production of proinflammatory cytokines by EP(-/-) macrophages in response to Toll-like receptor agonists was much lower, compared with WT macrophages, whose dysfunction in EP(-/-) macrophages was not compensated by the addition of the secreted form of EP. These findings, taken together, suggested that EP plays a critical role in immune/inflammatory-related responses of keratinocytes and macrophages at the barrier from the outside milieu and that the secreted and membrane-bound forms of EP have distinct functions.

Topics: Animals; Blastocyst; Dermatitis; DNA; Epidermal Growth Factor; Epiregulin; Exons; Genomic Library; Keratinocytes; Macrophages; Mice; Mice, Knockout; Restriction Mapping; Stem Cell Transplantation; Wound Healing