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. Polyvinyl chloride microplastics have been detected within clinical settings and may influence bacterial infections. Here, the authors demonstrate that these microplastics facilitate acute infection by uropathogenic E. coli, helping the bacteria evade immune cells and increase shedding.