Persistent inflammation in photo-aged skin

Photoaging is a major senescence process in human skin, with changes such as rough texture, elastosis, and irregular pigmentation. Previous reports demonstrated that repetitive ultraviolet B (UVB) exposure for several months evoked irreversible changes in hairless mice, similar to that noted in photoaged skin; thus, treated mice became a photoaging model. Although the photoaging mechanism remains unclear, prolonged inflammation due to repetitive UVB irradiation is the suspected cause. To further study photoaging, we compared UVB-exposed and unexposed skin in individual mice using half-body exposure to repetitive UVB. After 8 weeks, UVB-exposed areas had a faint reddish and swollen appearance, with loss of texture. This change persisted for more than 3 months after final exposure, and did not expand to involve peripheral areas. Persistent inflammation in the lesion was suggested by immunohistochemical analysis and observation of chronic reactive oxygen species (ROS) generation using a bioimager and intravenous injection of an ROS indicator. We next examined the distribution of phosphoglycerate mutase (PGAM), an aging marker that decreases in senescent cells. As expected, recruitment of fibroblasts and keratinocytes with specific decreases in PGAM was observed in the photoaged area, suggesting progression of cell aging. As we also noted decrease of PGAM in inflammatory skin lesions unaccompanied by photoaging, chronic inflammation might result in decreased PGAM in photoaged skin. These findings showed that chronic inflammation persisted in photoaged skin, and may evoke multiple changes along with progressive photoaging.