PVC microplastics facilitate uropathogenic Escherichia coli pathogenicity by enhancing host cell invasion and mitochondrial-dependent pyroptosis.

Microplastics (MPs), ubiquitous environmental pollutants, can enter the human body and exacerbate health risks. Polyvinyl chloride MPs (PVC-MPs) are emerging contaminants of particular concern due to direct clinical exposure pathway. However, the role of PVC-MPs in pathogenic bacterial infections remains poorly understood. Here, we investigate the role of PVC-MPs for the pathogenicity of uropathogenic Escherichia coli (UPEC), the primary causative agent of urinary tract infections (UTIs). Results demonstrate that PVC-MPs significantly enhance both acute and chronic UTIs. Mechanically, PVC-MPs act as carriers, enriching UPEC on their surface and enhancing UPEC invasion of bladder epithelial cells (BECs) via receptor-independent pathway, thereby promoting UPEC colonization in mouse bladders and kidneys. After entering BECs, intracellular PVC-MPs induce mitochondrial dysfunction, causing mitochondrial reactive oxygen species accumulation and mitochondrial DNA leakage, which activate Caspase-1-dependent pyroptosis, promoting urothelial cell shedding and UPEC chronic infection. These findings establish PVC-MPs as mediators of UTI pathogenesis, providing critical mechanistic insights into how environmental pollutant exposure may enhance susceptibility to infectious diseases.