Gut microbiota dysbiosis exacerbates polystyrene microplastics-induced liver inflammation via activating LPS/TLR4 signaling pathway in ducks.

Abstract

Ubiquitous microplastics can bioaccumulate in organisms, resulting in detrimental health impacts, such as liver inflammation. Nonetheless, the exact mechanism by which polystyrene microplastics (PS-MPs) trigger liver inflammation via the gut-liver axis in ducks remains unclear. The purpose of this study was to clarify the impact of PS-MPs exposure to liver inflammation through the gut-liver axis in ducks. Our investigation indicated that exposure to PS-MPs markedly upregulated the levels of MDA and ROS in the liver tissue and enhanced the release of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β). Additionally, PS-MPs exposure increased the LPS level, which ultimately triggered the TLR4/NF-κB signaling pathway. Notably, exposure to PS-MPs resulted in a marked change in the gut microbiota composition, primarily indicated by an increase in the relative abundance of Brachyspiraceae and a reduction in that of CAG-74 and Oscillospiraceae. Metabolome analysis further revealed that different expressed metabolites (DEMs) in the positive and negative mode were identified between the control and HMPs groups, including 1-methylhistamine, DL-Methionine sulfoxide, Guanidinoethyl sulfonate, l-Cysteic acid, Deoxyinosine, Camp. Both metagenomic and metabolome analyses showed enrichment in the lysosomal pathway. Correlation analysis suggested association among representative gut microbiota, serum LPS, oxidative stress factors, liver DEMs and key liver inflammatory indicators. Our study sheds light on the mechanism by which PS-MPs exposure induced liver inflammation in ducks via the modulation of the gut-liver axis. These findings improved our understanding of the underlying mechanisms that contribute to PS-MPs-induced hepatotoxicity in avian species.