title: Green tea polyphenol (-)-epigallocatechin-3-gallate treatment to mouse skin prevents UVB-induced infiltration of leukocytes, depletion of antigen-presenting cells, and oxidative stress.
abstract: Ultraviolet (UV) radiation-induced infiltrating leukocytes, depletion of antigen-presenting cells, and oxidative stress in the skin play an important role in the induction of immune suppression and photocarcinogenesis. Earlier we have shown that topical application of polyphenols from green tea or its major chemopreventive constituent (-)-epigallocatechin-3-gallate (EGCG) prevents UV-B-induced immunosuppression in mice. To define the mechanism of prevention, we found that topical application of EGCG (3 mg/mouse/3 cm(2) of skin area) to C3H/HeN mice before a single dose of UV-B (90 mJ/cm(2)) exposure inhibited UV-B-induced infiltration of leukocytes, specifically the CD11b+ cell type, and myeloperoxidase activity, a marker of tissue infiltration of leukocytes. EGCG treatment was also found to prevent UV-B-induced depletion in the number of antigen-presenting cells when immunohistochemically detected as class II MHC+ Ia+ cells. UV-B-induced infiltrating cell production of H2O2 and nitric oxide (NO) was determined as a marker of oxidative stress. We found that pretreatment of EGCG decreased the number of UV-B-induced increases in H2O2-producing cells and inducible nitric oxide synthase-expressing cells and the production of H2O2 and NO in both epidermis and dermis at a UV-B-irradiated site. Together, these data suggest that prevention of UV-B-induced infiltrating leukocytes, antigen-presenting cells, and oxidative stress by EGCG treatment of mouse skin may be associated with the prevention of UV-B-induced immunosuppression and photocarcinogenesis.
authors.affiliation: Department of Dermatology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. skatiyar@uab.edu
authors.forename: S K
authors.initials: SK
authors.lastname: Katiyar
authors.forename: H
authors.initials: H
authors.lastname: Mukhtar
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000187:drug effects* / Q000276:immunology / Q000528:radiation effects; D000975:Antioxidants / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives / Q000494:pharmacology*; D005260:Female; D005419:Flavonoids; D006861:Hydrogen Peroxide / Q000378:metabolism; D007962:Leukocytes / Q000187:drug effects* / Q000276:immunology / Q000528:radiation effects; D051379:Mice; D008809:Mice, Inbred C3H; D020556:Neutrophil Infiltration; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II; D018384:Oxidative Stress; D010636:Phenols / Q000494:pharmacology*; D011108:Polymers / Q000494:pharmacology*; D012867:Skin / Q000187:drug effects* / Q000276:immunology / Q000528:radiation effects; D013662:Tea; D014466:Ultraviolet Rays
chemical_list: D000975:Antioxidants; D005419:Flavonoids; D010636:Phenols; D011108:Polymers; D013662:Tea; D009569:Nitric Oxide; D002392:Catechin; D006861:Hydrogen Peroxide; C045651:epigallocatechin gallate; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse