Chronic exposure to UVB induces nephritis and gut microbiota dysbiosis in mice based on the integration of renal transcriptome profiles and 16S rRNA sequencing data.

Ultraviolet (UV) is a common and abundant environmental factor that affects daily life. Although the effects of UV radiation on the skin have been extensively reported, studies on the influence of UV radiation on internal organs are still limited. This study aimed to evaluate the influence of UVB exposure on the kidney of mice and to investigate the possible mechanism. In the present study, histopathology changes, oxidative stress, and inflammatory response were used to evaluate the kidney and colon injury induced by UVB exposure. The results showed that the 14-week chronic skin exposure to UVB triggers a kidney injury response characterized by macrophage infiltration, elevated oxidative stress as well as inflammatory and injury markers. The RNA sequencing demonstrated that chronic UVB exposure could alter the kidney transcriptomic profile distinguished by the regulation of genes involved in the Notch signaling pathway, JAK-STAT signaling pathway, and ECM-receptor interaction. Besides, chronic UVB exposure also resulted in gut dysbiosis, manifested as colon macrophage infiltration, stimulated inflammatory responses, impaired barrier integrity, and microbiota structural and functional disorders. The Spearman analysis results further revealed a strong correlation between gut microbiota and kidney injury. In conclusion, skin chronic exposure to UVB causes nephritis and gut microbiota dysbiosis in mice, and these findings provide new insight into the underlying risks of chronic UVB exposure to human wellness. [Display omitted] • Mice chronic exposure to UVB induced renal inflammation and colonic injury. • More than 1700 DEGs were identified by RNA-seq in kidneys of UVB-irradiated mice. • Chronic UVB exposure upregulated Notch, JAK-STAT, and ECM pathways in the kidneys. • Chronic UVB exposure altered the gut microbiota structure and function in mice. [ABSTRACT FROM AUTHOR]