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Updated: Aug 2, 2026
Protocol for Microplastics Sampling on the Sea Surface and Sample Analysis
Published on: December 16, 2016
Polystyrene microplastics promote liver inflammation by inducing the formation of macrophages extracellular traps
Kai Yin1, Dongxu Wang1, Yue Zhang1
1College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Abstract:
Microplastics (MPs), a new and increasing environmental pollutant, can cause ongoing damage to organisms. Although recent studies have revealed mechanisms of action for some of the hepatotoxicity caused by MPs, the role-played by cellular interactions, particularly immune cells, in the process of liver injury has not been elucidated. In the present study, 5-μm polystyrene microplastics (PS-MPs) induced liver inflammation as well as the formation of Macrophage extracellular traps (METs). Macrophage and LMH cell co-culture systems confirmed that PS-MPs-induced METs promote inflammation in hepatocytes. Mechanistically, macrophages actively phagocytose particles after 4 h of exposure to PS-MPs. Subsequently PS-MPs elevated ROS levels and disrupt mitochondrial kinetic homeostasis. Further activation of mitochondrial autophagy and lysosomes. After phagocytosis of PS-MPs by macrophages for 12 h, continued autophagy and lysosome activation eventually lead to lysosome rupture and release of calcium ions to induce the formation of METs. Blocking ROS (NAC) and autophagy (3MA) partially alleviated mitochondrial and lysosomal damage and thus inhibited the formation of METs induced by PS-MPs. NAC also delayed the onset of respiratory burst to alleviate METs formation. In conclusion, our study reveals the mechanism of METs formation in liver inflammation induced by PS-MPs exposure and suggests that lysosomal damage may be one of the key players in the formation of METs induced by PS-MPs.
Insights
Polystyrene microplastics (PS-MPs) trigger liver inflammation by causing macrophages to form extracellular traps (METs). Lysosomal damage and calcium ion release are key steps in this inflammatory process.
Area of Science:
- Environmental Science
- Toxicology
- Cell Biology
Background:
- Microplastics (MPs) are emerging environmental pollutants causing organismal damage.
- Hepatotoxicity mechanisms of MPs are partially understood, but immune cell roles in liver injury remain unclear.
Purpose of the Study:
- To elucidate the role of cellular interactions, specifically immune cells, in microplastic-induced liver injury.
- To investigate the mechanism of Macrophage Extracellular Trap (MET) formation induced by polystyrene microplastics (PS-MPs).
Main Methods:
- Utilized macrophage and LMH cell co-culture systems to study PS-MP effects.
- Investigated cellular responses including phagocytosis, reactive oxygen species (ROS) levels, mitochondrial homeostasis, autophagy, and lysosomal activity.
- Employed ROS inhibitor (NAC) and autophagy inhibitor (3MA) to block specific pathways.
Main Results:
- 5-μm PS-MPs induced liver inflammation and Macrophage Extracellular Trap (MET) formation.
- PS-MPs activated macrophages, leading to elevated ROS, disrupted mitochondrial homeostasis, and subsequent autophagy and lysosome activation.
- Lysosome rupture and calcium ion release were identified as crucial for MET formation; blocking ROS and autophagy partially inhibited this process.
Conclusions:
- PS-MPs induce liver inflammation through MET formation, involving macrophage activation and cellular damage.
- Lysosomal damage and calcium ion release are critical mediators in PS-MP-induced MET formation.
- Targeting ROS and autophagy pathways may offer therapeutic strategies against microplastic-induced liver injury.
