Ultraviolet B (UVB) radiation induces inflammation in the skin specifically at the site of exposure. We unexpectedly found that UVB-induced inflammation was not induced in gp91phox-depleted mice. To test whether gp91phox is directly involved in UVB-induced inflammation, neutrophil- and hyaluronic acid-depleted mice were also irradiated and examined for their response. Hyaluronic acid-depleted mice showed strongly inhibited UVB-induced inflammation, but the neutrophil-depleted mice did not exhibit any suppressed UVB-induced inflammation. To elucidate the pathway by which UVB irradiation induced inflammation, we examined the expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) and caspase-1 in the mouse skin. An increase in the expression of NLRP3 and caspase-1 was seen following the UVB irradiation of C57BL mice; however, the UVB-irradiated gp91phox-knockout (gp91phox(-/-)) mice did not have this increase in expression. Furthermore, the plasma IL-1β level increased after the UVB irradiation in C57BL mice, but there was no change in the gp91phox(-/-) mice. These results clearly indicate that nicotinamide adenine dinucleotide phosphate oxidase is activated by gp91phox, which is expressed on the surface in response to the increased expression of hyaluronic acid induced by UVB irradiation, and as result, the generation of reactive oxygen species (ROS) increases. This ROS activate NLRP3, and NLRP3 leads to the production of caspase-1, which subsequently increases IL-1β, thereby finally inducing inflammation. It is thought that this system may play an important role in the damage and ageing of skin, and further studies are necessary to confirm these finding.

Irradiation by ultraviolet A (UVA) initiates the suppression of skin contact hypersensitivity. However, the change in the whole body immunity by UVA irradiation of the eye is still unknown. The mice used in this study were separated into four groups namely: a control, UVA irradiation of the eye, UVA irradiation of the ear, UVA irradiation of the eye + a glucocorticoid receptor antagonist (RU-486) administrated, UVA irradiation of the eye with an adrenalectomy and non-irradiation + cortisol administrated groups. The eye or ear was locally exposed to UVA after covering the remaining body surface with aluminum foil at a dose of 110 kJ/m(2) using a FL20SBLB-A lamp. Plasma adrenocorticotropic hormone, cortisol, and interleukin-10 (IL-10) content increased by UVA irradiation of the eye. In addition, UVA irradiation of the eye induced down-regulation of the epidermal Langerhans cells in the ear and the up-regulation of the mucosal immunoglobulin A (IgA) in the intestine. However, the changes in the epidermal Langerhans cells and mucosal IgA of UVA irradiation of the eye are not induced either by the RU-486 treatment or an adrenalectomy. These results clearly indicate that the signal evoked by UVA irradiation of the eye, through the hypothalamo-pituitary-adrenal pathway, up-regulated the production of glucocorticosterone. This hormone controls immunity, and the possibility that it performed a living body defense for UVA exposure was thus suggested.

These results clearly indicate that tranexamic acid decreases the expression of PC2, which cleavages from proopiomelanocortin to α-MSH in the pituitary gland, thereby suppressing melanocyte activation.

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Ultraviolet (UV) eye irradiation denatures the cells of the intestine. This study examined the action of UVA and UVB on dextran sodium sulfate (DSS)-induced ulcerative colitis. We produced a mouse model of ulcerative colitis by administering DSS for 5 days and irradiated the eye with UVB or UVA for each day of the DSS treatment period. DSS-induced ulcerative colitis was deteriorated by the UVB eye irradiation. Conversely, the symptoms improved with UVA eye irradiation. The levels of adrenocorticotropic hormone (ACTH), corticotropin-releasing hormone (CRH), urocortin 2, interleukin (IL)-18, IL-6 and histamine in the blood increased after the UVB eye irradiation of DSS-treated mice (UVB/DSS-treated mice). In contrast, the β-endorphin level in the blood of the UVA/DSS-treated mice increased and the levels of urocortin 2, tumor necrosis factor (TNF)-α and histamine decreased. Furthermore, in the colon, the expression of melanocortin-2 receptors (MC2R) increased in the UVB/DSS-treated mice, while the expression of μ-opioid receptors increased in the UVA/DSS-treated mice. When an ACTH inhibitor was administered, UVB eye irradiation caused the deterioration of DSS-treated ulcerative colitis, while the effect of UV eye irradiation disappeared with a μ-opioid receptor antagonist. These results suggested that UV eye irradiation plays an important role in DSS-induced ulcerative colitis.