Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota–gut–brain axis in mice

Abstract

The remarkably increase in plastic use has led to worldwide pollution involving microplastics (MPs), which have been shown to be potentially hazardous substances. Although several studies have focused on the effects of small MPs on the brain and behavior of aquatic species, their effects on the mouse brain and the underlying mechanisms remain unclear. Our study’s aim was to investigate the effects of long-term oral ingestion of different sizes of MPs (0.1, 5, and 50 μm) on mouse colon tissue. Of these sizes, the smallest (0.1 μm) had the greatest effect. Pre-administration of MP promotes colitis but reduces tumor growth in a colitis-associated colorectal cancer (CAC) mouse mode. MPs can increase inflammation in mice via activation of the very late antigen 4–vascular cell adhesion molecule 1 (VLA4-VCAM1) signaling pathway in macrophages, while also inducing macrophage reduction in the late phase of inflammation. In the microbiota–gut–brain axis, polystyrene MP treatment altered bile acid and carbohydrate metabolism in the intestine, inhibited intestinal motility, reduced water reabsorption, and led to a certain degree of depression in mice. These findings suggest that small MPs can induce macrophage reduction, thereby affecting the physical and mental health by modulating the microbiota–gut–brain axis. • Microplastics increased intestinal permeability and inflammation in mice. • The intake of microplastics altered the structure of the gut microbiome in mice. • These microbiome changes affected bile acid and carbohydrate metabolism in the gut. • Long-term intake of microplastics led to macrophage depletion. • Microplastics exerted effects via modulation of the microbiome–gut–brain axis.

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