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Abstract: Infrared radiation is a substantial part of the solar energy output reaching the earth surface. Therefore, exposure of humans to infrared radiation is common. However, whether and how infrared (IR) or infrared A acts on human skin cells is still under debate. Recently the generation of reactive oxygen species by water-filtered infrared A (wIRA) irradiation was postulated. wIRA shows a spectral distribution similar to that of solar irradiation at the earth''s surface. Thus, the need for protection of human skin from both solar- and artificially generated infrared A irradiation was concluded. Here we demonstrate that in human dermal fibroblasts this reactive oxygen species generation is dependent on heat formation by infrared A and can be reproduced by thermal exposure. On the other hand wIRA irradiation had no detectable effect if the temperature in the cells was kept constant, even if irradiance exceeded the extraterrestrial solar irradiance in the IR range by a factor of about 4 and the maximum at noontime in the tropics by a factor up to about 6. This could be demonstrated by the measurement of oxidant formation using H2DCFDA and the determination of protein carbonyls. In additional experiments we could show that during thermal exposure the mitochondria contribute significantly to oxidant production. Further experiments revealed that the major absorbance of infrared is due to absorption of the energy by cellular water. [Copyright &y& Elsevier]

A computational model of both the absorbed radiation and transient temperature fields in multilayer superficial human tissues in the case of an external water-filtered infrared-A irradiation is developed. A novel simplified model for radiative transfer is based on local 1-D solutions taking into account the oblique incidence of radiation at the periphery of the heated region. The computational study of a model problem at typical geometrical, optical, and thermal parameters confirms the acceptable accuracy of the 1-D solution for the temperature field formed in human tissues during thermal treatment with periodic infrared irradiation. The effects of uncertainties in spectral absorption coefficients and thermal conductivity of biological tissues on thermal treatment parameters are analyzed. It is shown that the temperature response to periodic water-filtered infrared-A heating can be used to estimate optical properties of human tissues. The calculations show that the decrease in convective heat transfer with the heating of air in the gap between the radiation source and the body surface has to be taken into account. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) irradiation is an established treatment for inflammatory skin diseases, although the precise mode of action is still unclear. Activating and suppressive effects on mast cell (MC) mediator release have been described. The aim of this study was to investigate systematically the effects of UVB, UVA-1, and psoralen plus UVA-1 at therapeutic doses on skin-derived human MC. Baseline and stimulated release of histamine, tryptase, and of interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha (TNF-α) were examined. In resting MC, UV light induced a slight, yet significant histamine release corresponding to enhanced surface levels of lysosome-associated membrane proteins (LAMP). In contrast, UV pre-treatment caused a marked suppression of the anti-IgE-induced histamine release, accompanied by a diminished, anti-IgE-mediated increase in LAMP expression. The secretion of IL-6, IL-8, and TNF-α was inhibited in resting and activated MC, suggesting a different mode of action. Regarding the importance of MC in a variety of allergic and inflammatory processes, our data show a high susceptibility of this cell type towards UV light, which seems to partially depend on the state of cellular activation. Immunosuppressive effects predominate in activated MC, thus corresponding with the beneficial effects in inflammatory diseases, whereas in resting MC, both stimulatory and inhibitory effects are observed. [ABSTRACT FROM AUTHOR]

Ultraviolet irradiation represents a well-established treatment modality for inflammatory skin diseases. The aim of this study was to investigate the mechanisms of ultraviolet B radiation-induced keratinocyte insensitivity towards interferon-γ. Flow cytometric analyses indicated that ultraviolet B radiation temporarily inhibits the interferon-γ-induced activation of primary keratinocyte and HaCaT cells as measured by reduced intercellular adhesion molecule-1 (CD54) and HLA-DR upregulation. Western blot experiments have suggested that this is mediated by the ultraviolet B radiation-induced inhibition of signal transduction and transcription factor-1 phosphorylation. Neither interleukin-10 neutralization nor interleukin-10 addition had any effect on the ultraviolet B radiation-induced inhibition of interferon-γ induced intercellular adhesion molecule-1 expression. Furthermore, the supernatant from ultraviolet B-irradiated cells failed to inhibit the interferon-γ-induced CD54 and HLA-DR upregulation in nonradiated HaCaT cells. Moreover, irradiated cells from whom the supernatant was withdrawn 4 h after irradiation still showed a diminished interferon-γinduced response after 24 h. Thus, not soluble but intracellular factors might be involved in the ultraviolet B radiation-induced inhibition of interferon-γ-induced keratinocyte activation. Therefore, we analyzed the expression of members of suppressors of cytokine-signaling (SOCS) molecules using real-time polymerase chain reaction. We found a fast and strong upregulation of SOCS1 and SOCS3 but not of SOCS2 after ultraviolet B radiation. Similarly, ultraviolet B radiation induced the expression of these particular SOCS molecules in lesional psoriatic skin. As SOCS molecules are known inhibitors of signal transduction and transcription factor phosphorylation, which is essential for interferon-γ-induced intercellular adhesion molecule-1 and HLA-DR upregulation, this may explain the interferon-γ unresponsiveness after ultraviolet B radiation. [ABSTRACT FROM AUTHOR]