Prevention of UVB-induced immunosuppression in mice by the green tea polyphenol (-)-epigallocatechin-3-gallate may be associated with alterations in IL-10 and IL-12 production

Citation
Sk. Katiyar et al., Prevention of UVB-induced immunosuppression in mice by the green tea polyphenol (-)-epigallocatechin-3-gallate may be associated with alterations in IL-10 and IL-12 production, CARCINOGENE, 20(11), 1999, pp. 2117-2124
Citations number
52
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
CARCINOGENESIS
ISSN journal
01433334 → ACNP
Volume
20
Issue
11
Year of publication
1999
Pages
2117 - 2124
Database
ISI
SICI code
0143-3334(199911)20:11<2117:POUIIM>2.0.ZU;2-W
Abstract
UV exposure of the skin, particularly UVB (290-320 nm), causes adverse biol ogical effects, including alterations in cutaneous immune cells, photoaging and photocarcinogenesis. Several studies have shown that polyphenolic comp ounds isolated from green tea afford protection against UVB-induced inflamm atory responses and photocarcinogenesis in murine models. In this study we show that topical application of (-)-epigallocatechin-3-gallate (EGCG) (3 m g/mouse), a major polyphenolic component of green tea, before a single low dose UVB exposure (72 mJ/cm(2)) to C3H/HeN mice prevented UVB-induced inhib ition of the contact hypersensitivity response and tolerance induction to t he contact sensitizer 2,4-dinitrofluorobenzene, Topical application of EGCG before UVB exposure reduced the number of CD11b+ monocytes/macrophages and neutrophils infiltrating into skin inflammatory lesions, which are conside red to be responsible for creating the UV-induced immunosuppressive state. In addition, application of EGCG before UVB exposure decreased UVB-induced production of the immunomodulatory cytokine interleukin (IL)-10 in skin as well as in draining lymph nodes (DLN), whereas production of IL-12, which i s considered to be a mediator and adjuvant for induction of contact sensiti vity, was found to be markedly increased in DLN when compared with UVB alon e-exposed mice. Taken together, our data demonstrate that EGCG protects aga inst UVB-induced immunosuppression and tolerance induction by: (i) blocking UVB-induced infiltration of CD11b+ cells into the skin; (ii) reducing IL-1 0 production in skin as well as in DLN; (iii) markedly increasing IL-12 pro duction in DLN, Protection against UVB-induced immunosuppression by EGCG ma y be associated with protection against UVB-induced photocarcinogenesis.