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1 March 2003 CD11b Cells are the Major Source of Oxidative Stress in UV Radiation–irradiated Skin: Possible Role in Photoaging and Photocarcinogenesis
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Abstract

Exposure of skin to solar UV radiation induces oxidative stress and suppression of cell-mediated immune responses. These effects are associated with the greater risk of several skin disorders including photoaging and photocarcinogenesis. We have shown that UV-induced infiltrating leukocytes contribute in developing oxidative stress in UV-irradiated skin. The peak period of UV-induced infiltrating leukocytes lies between 48 and 72 h after UV exposure of the skin. In this study we demonstrated that UV (90 mJ/cm2)-induced infiltrating CD11b cells in C3H/HeN mice skin were the major source of oxidative stress. Hydrogen peroxide (H2O2) was determined as a marker of oxidative stress. Flow cytometric analysis of viable cells revealed that the number of CD11b H2O2 cells were significantly higher (31.8%, P < 0.001) in UV-irradiated skin in comparison with non–UV-exposed skin (0.4%). Intraperitoneal administration of monoclonal antibodies to CD11b (rat IgG2b) to C3H/HeN mice inhibited UVB-induced infiltration of leukocytes, as evidenced by reduction in myeloperoxidase activity (64–80%, P < 0.0005), concomitant with significant reduction in H2O2 production both in epidermis and dermis (66–83%, P < 0.001–0.0005) when compared with the administration of rat IgG2b isotype of anti-CD11b. Furthermore, CD11b and CD11b− cell subsets were separated by immunomagnetic cell isolation technique from total epidermal and dermal single cell suspensions obtained 48 h after UV irradiation of the skin and analyzed for H2O2 production. Analytical data revealed that CD11b cell population from UV-irradiated skin resulted in significantly higher production of total H2O2 in both epidermis and dermis (87–89%, P < 0.0001) in comparison with CD11b− cell population (11–13% of total H2O2). These data revealed that infiltrating CD11b cells were the major source of oxidative stress in UV-irradiated skin and thus may contribute to photoaging and promotion of skin tumor growth within the UV-irradiated skin. Together, these data suggest that reduction in UV-induced skin infiltration of CD11b cells may be an alternative and effective strategy to reduce solar UV light–induced oxidative stress–mediated skin disorders including photoaging and photocarcinogenesis.

Anshu Mittal, Craig A. Elmets, and Santosh K. Katiyar "CD11b Cells are the Major Source of Oxidative Stress in UV Radiation–irradiated Skin: Possible Role in Photoaging and Photocarcinogenesis," Photochemistry and Photobiology 77(3), 259-264, (1 March 2003). https://doi.org/10.1562/0031-8655(2003)077<0259:CCATMS>2.0.CO;2
Received: 25 July 2002; Accepted: 1 December 2002; Published: 1 March 2003
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