Fig. 8

ZnONPs disrupt lysosome activity and impair autophagic flux to facilitate exosome secretion in keratinocytes and macrophages. Under UVB exposure, ZnONPs lead to autophagosome accumulation and lysosome dysfunction, which activate the NLRP3 inflammasome and enhance the release of exosomes by HaCaT cells. Moreover, exosomes secreted by HaCaT cells stimulated M1 macrophage activation, and further exposure to ZnONPs upregulated the NFκB signaling pathway and NLRP3 inflammasome-autophagy-exosomal pathway. Cytokines and exosomes released from macrophages further accelerated inflammatory responses in keratinocytes, which affected UVB-induced skin injury