Photo-dermatology最新文献

The effect of ultraviolet light B (UVB) on immediate and delayed irritant reactions induced by dimethyl sulphoxide (DMSO), phenol, and sodium lauryl sulphate (SLS) was studied in 12 volunteers. One half of the upper back was irradiated with 0.16 J/cm2 of UVB. Patch tests for immediate reactions were performed using dilution series of test substances on the 3rd, 9th and 15th days and for delayed reactions on the 2nd, 8th and 14th days after irradiation both on the UV-exposed and non-exposed areas of the back. The occlusion time was 20 min for immediate reactions and 20 h for delayed ones. Changes in the skin blood flow of the test sites were monitored using laser-Doppler flowmetry, and erythema and edema reactions were observed visually. Both immediate and delayed reactions were caused by DMSO and phenol; SLS elicited only delayed reactions. UVB diminished immediate reactions induced by phenol for at least 15 days after irradiation. Immediate reactions to DMSO were diminished 40 min after application on the UV-exposed area on the 3rd day. UVB diminished the delayed reactions from SLS and DMSO but not reactions induced by phenol.

Using an in vivo skin chamber method, we demonstrated increased release of interleukin-1 (IL-1)-like activity at the site of irradiation with 3 times the minimal erythema dose of ultraviolet B (UVB). IL-1-like activity was estimated using the mouse thymocyte amplification assay. UVB-augmented release of IL-1-like activity peaked 1 h after irradiation and levels returned to baseline by 2 h. Release of IL-1-like activity from human skin after exposure to UV radiation may account for some of the local and systemic features of the sunburn response.

UV irradiation is known to photoisomerize epidermal trans-urocanic acid (trans-UCA) to cis-urocanic acid (cis-UCA), which has been postulated to be involved in local and systemic downregulation of immune responses. We have earlier shown that cis-UCA suppresses interleukin 1 (IL-1) production in human epidermal cells. To study the possible effects of UCA isomers on human peripheral blood lymphoid cells, these cells were cultured in the presence of either UCA stereoisomer, and a number of immunological parameters were assayed. Cis-UCA (100 micrograms/ml) caused a significant downregulation of monocyte IL-1 production, and diminished monocyte HLA-DR expression. Cis-UCA also caused a significant reduction in the CD4/CD8 ratio. Furthermore, T-cells preincubated with cis-UCA caused a significant downregulation of purified protein derivative-induced interleukin 2 production by autologous T-cells. The trans isomer had no effect in any of these in vitro tests. The reported stereospecific effects of cis-UCA are compatible with the postulated function of this chemical as an UV-induced, low-molecular-weight immunomediator substance.

New light has recently been shed on the way phototherapy reduces bilirubin concentration in icteric infants. The introduction of a high-performance liquid chromatography technique led to the discovery of new photoisomers of bilirubin, the configurational and structural isomers with high and low quantum yields, respectively, and to a renewed interest in the photochemical properties of bilirubin in vitro and in vivo. Circular dichroism and absorption spectroscopies have then shown that bilirubin behaves like a bichromophoric system, with the 2 halves of the molecule strongly interacting in the excited state. This coupling mechanism makes the quantum yields of bilirubin photochemistry wavelength-dependent, with marked effects in the long wavelength edge of the bilirubin absorption spectrum. The photochemistry of bilirubin is substantially similar in icteric rats and babies, and is consistent with what is observed in vitro. However, the metabolism of bilirubin photoproducts in rats sometimes differs quite significantly from that in babies. In particular, only the low quantum yield structural isomer, lumirubin, is efficiently excreted by babies. Although the relative role of the bilirubin photoprocesses in the therapy of hyperbilirubinemia is not yet known with certainty, the structural photoisomerization is generally assumed to represent the main route of bilirubin elimination. As a consequence, the determination of the spectral band that optimizes the process of formation of lumirubin in neonate may represent an important step in the improvement of the clinical protocol of phototherapy. Therefore, in addition to reviewing the most recent data on bilirubin photochemistry and the metabolism of bilirubin products, this article presents a computation of the optimal light for lumirubin formation. The combined effects of long-wavelength photochemistry of bilirubin and skin attenuation show that the optimal spectral range should be between 480 and 510 nm.

Many skin diseases, such as graft-versus-host disease (GVHD), are marked by lymphocyte infiltrates in the skin. Severity of these diseases is often correlated with the induced expression of class II antigens (human, HLA-DR,; murine, Ia) by the keratinocytes. This suggests that HLA-DR-expressing keratinocytes may be involved in the pathogenesis of these diseases. Since some of these diseases are effectively treated with ultraviolet radiation (UVR), this study was conducted to determine whether UVR alters the keratinocyte expression of class II antigens. To test this hypothesis, 2 models of experimentally induced keratinocyte Ia expression were employed. First, athymic nude mice with one ear protected by electrical tape were exposed to UVR (450 J/m2/day on 4 consecutive days). They were then given an i.v. injection of normal mouse serum (NMS) to induce keratinocyte Ia expression. Keratinocytes in the UVR-exposed skin of these animals were not induced to express Ia; however, Ia-expressing keratinocytes were observed in the epidermis of shielded skin sites. Likewise, it was determined that UVR was capable of downregulating keratinocyte expression of Ia when administered to nude mice 7 d after receiving an injection of NMS. Second, employing a clinically relevant model, we found that Ia expression by keratinocytes in mice undergoing experimentally induced GVHD was abrogated by UVR treatment. This appeared to be a direct effect of the UVR, since keratinocytes in shielded skin sites and mucosal cells in the intestinal epithelium of animals with GVHD were shown to express Ia. These data provide compelling evidence for our hypothesis that decreased HLA-DR expression by keratinocytes in diseased skin treated with UVR is a mechanism by which UVR exerts its therapeutic effect.

A solution of para-aminobenzoic acid (PABA) was exposed to ultraviolet (UV) radiation emitted from a Philips TL 40 W/12 sunlamp and the degree of photodegradation following an exposure of 27 J/cm2 was estimated to be approximately 40%. The formation of the photoproducts was confirmed by mass spectroscopy and UV spectroscopy. The solution was painted on the backs of hairless light-pigmented mice prior to daily UV irradiation by the above sunlamp, and this procedure was continued for 30 weeks. The preirradiated solution of PABA significantly retarded the tumor induction time and reduced significantly the number of squamous cell carcinomas compared with nonprotected controls. This tumor-retarding ability did not differ significantly from the effect achieved when using nonirradiated PABA.

The interaction between ultraviolet A (UVA) and ultraviolet B (UVB) on erythemal reaction was investigated on the skin of the backs of 24 healthy Japanese volunteers, using narrow-band radiation. The minimal erythema doses (MED) for UVB (MEDB) and UVA (MEDA) were determined and UVA and UVB were both applied to the same site in immediate combination with 2 orders of exposure (A + B, B + A). In experiment 1 the interaction between suberythemogenic doses of UVA and UVB to produce a visible erythema was examined; the sum of the fraction of MEDA and the fraction of MEDB was at most equal to 1 for 3 different doses of UVA (1, 2.4, 4.9 J/cm2) with either order of exposure. This interaction is considered to be photoaddition. In experiment 2 a fixed dose of UVB (1.7 MEDB of each subject) was applied in combination with 4 different doses of UVA (1, 2.4, 4.9, 7.4 J/cm2); the erythemal reaction was compared with the grading scale erythema produced by UVB alone and allotted a score of 1 to 7. The total number of MED irradiated was calculated for each combination exposure and the score obtained was compared with the score expected on the basis of that number of MED. The scores for A + B practically coincided with the expected values, whereas those for B + A were decidedly smaller than the expected values. This suggests photoaddition for A + B and photorecovery for B + A in the bright erythema dose range. The relationship between the Japanese skin type (JST) and the waveband interaction was also examined. In experiment 2, when UVA irradiation was followed by UVB, the subjects in JST group III showed photorecovery for high-dose UVA.