Oral feeding of nanoplastics affects brain function of mice by inducing macrophage IL-1 signal in the intestine

Nanoplastics (NPs) as contaminants in food and water have drawn increasing public attention. However, little is known about how NPs shape the gut immune landscape after injection. In this study, we fabricate NPs (-500 nm) and microplastics (MPs) (-2 mm) and evaluate their in vivo effects by feeding them to mice. The results suggest that NPs show a better ability to induce gut macrophage activation than MPs. In addition, NPs trigger gut interleukin-1 (IL-1)-producing macrophage reprogramming via inducing lysosomal damage. More importantly, IL-1 signaling from the intestine can affect brain immunity, leading to microglial activation and Th17 differentiation, all of which correlates with a decline in cognitive and short-term memory in NP-fed mice. Thus, this study provides insight into the mechanism of action of the gut-brain axis, delineates the way NPs reduce brain function, and highlights the importance of fixing the plastic pollution problem worldwide.

Automated summary

This study investigates the effects of nanoplastics (NPs) on the gut immune landscape and brain immunity. The results demonstrate that NPs have a stronger impact on gut macrophage activation compared to microplastics (MPs). Moreover, NPs induce the reprogramming of gut interleukin-1 (IL-1)-producing macrophages through lysosomal damage, leading to microglial activation and Th17 differentiation in the brain, resulting in cognitive decline and short-term memory impairment in NP-fed mice. These findings provide insight into the mechanism of the gut-brain axis and highlight the global importance of addressing plastic pollution.