Polystyrene nanoplastics promote inflammation and aging in young mice via oral-gut microbiome disruption

The escalating global presence of nanoplastics (NPs) poses a significant, yet poorly understood, threat to organismal health. Specifically, the impact of these ubiquitous pollutants on the crucial oral-gut microbiota axis and its subsequent role in driving systemic inflammation and aging in young organisms remains largely undefined. Current research highlights the gut microbiota's pivotal role in host health regulation, with dysbiosis linked to various age-related pathologies. Understanding how nanoplastics interfere with this delicate balance is critical, as existing knowledge on their toxicity mechanisms, particularly concerning the microbiome, is limited, leaving a substantial gap in developing preventive strategies.

Researchers investigated the effects of polystyrene nanoplastics (PS-NPs) on inflammation and aging in young mice. They established a free-feeding model using 8-week-old C57BL/6 mice, exposing them to 1000 μg/L PS-NPs via drinking water. The study assessed PS-NPs-induced inflammatory and aging effects by quantifying tissue inflammatory cytokines using ELISA and cellular senescence markers (p21Cip1/Waf, p16Ink4a) via qPCR. Additionally, 16S rRNA sequencing was employed to characterize structural changes in both oral and gut microbiota, providing insights into the disruption of the oral-gut axis. A control group received unadulterated drinking water.

Exposure to polystyrene nanoplastics (PS-NPs) significantly impacted young mice, inducing markers of both cellular senescence and inflammation. PS-NPs exposure significantly increased the expression levels of cellular senescence markers p21Cip1/Waf and p16Ink4a in both lung and liver tissues. Concurrently, the study found that PS-NPs promoted the release of key inflammatory cytokines, including IL-1β, IL-6, and TNF-α, by modulating the p38 MAPK pathway. Furthermore, PS-NPs also led to a decreased expression of antioxidant genes, suggesting impaired cellular defense mechanisms. The 16S rRNA sequencing analysis revealed that PS-NPs exposure caused significant dysbiosis in both oral and intestinal microbiota. This dysbiosis was manifested as significant alterations in microbial diversity and community structure, indicating a profound disruption of the oral-gut axis. These changes underscore a direct link between nanoplastic exposure and systemic physiological perturbations.

PS-NPs exposure significantly increased cellular senescence markers p21Cip1/Waf and p16Ink4a in lung and liver, alongside elevated inflammatory cytokines IL-1β, IL-6, and TNF-α via p38 MAPK modulation.