Abstract

Background: Microplastic (MP) is defined as the plastics size less than <5mm. MP accumulates in humans via ingestion. Therefore, the gut-liver axis may be a important to prevent MP accumulation. However, many of the studies focus on the marine organisms and its biological effect and distribution pattern remain to be elucidated in mammals. Therefore, the present study investigates the role of gut-liver axis in protection of hepatic MP accumulation.

Methods: During the experiment, mice were divided into control, control + MP, EtOH, and EtOH + MP groups. EtOH groups were ingested Lieber-deCarli ethanol diet for 5 weeks. Polystyrene (PS)-MP groups were orally administered at a dose of 0.1mg/kg 5 times a week. Since PS-MPs were tagged with immunofluorescent dye, the distribution pattern of MPs was analyzed with immunofluorescence assay. Liver injury was assessed with histopathology, serum ALT, AST, and TG assay, Oil-Red-O staining, and hepatic TG assay. Caco-2 was also used to analyze the MP distribution pattern under the similar condition as in vivo.

Results: EtOH + MP group showed the higher hepatic steatosis and inflammatory lesions than other groups. Moreover, EtOH + MP group showed significant higher MP accumulation than control + MP group, indicating that MP accumulation was affected by hepatic damage. To explore the mechanism, MP accumulation pattern in the intestines was next investigated since gut-liver axis is one of the key mechanisms in alcoholic liver disease. EtOH + MP group exhibited significant intestinal damages such as epithelial necrosis, vacuolar degeneration, disintegration and detachment, and fusion of villi. However, control + MP group showed intact intestinal structure. Similar with the histopathological patterns, EtOH + MP group showed a remarkably higher MPs accumulation pattern in the intestines than in control + MP group. In confocal images, MPs penetrated into the lamina propria through the damaged intestinal epithelium in EtOH + MP group while only few MPs penetrated in control + MP group, which was characterized by intact intestinal epithelial structure. Ethanol ingestion disrupted the intestinal mucosal barrier, and the PS-MP accumulation was remarkably increased.

Conclusion: The result suggests that ethanol aggravates PS-MPs accumulation in the liver via disrupted intestinal mucosal barrier, and the gut-liver axis could be a novel therapeutic target in prevention of PS-MPs accumulation in the body.