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Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
Host-Derived Intestinal Extracellular Vesicles Inhibit Polystyrene Microplastic-Induced Activation of Inflammation
Runze Wang1, Chaoqiao Wang1, Binjin Hu1
1School of Laboratory Medicine, Hangzhou Medical College, Hangzhou310053, Zhejiang, China.
Abstract:
Polystyrene microplastics (PS-MPs), as pervasive environmental contaminants, infiltrate the human body primarily via the food chain and accumulate in intestinal tissues, where they provoke inflammatory responses and disrupt cellular homeostasis. Although intestinal epithelial cell-derived extracellular vehicles (I-EVs) are recognized for their regulatory roles in maintaining gut integrity, their potential protective effects against PS-MP-induced intestinal inflammation and autophagy remain poorly understood. In this study, we investigated the impact of host-derived I-EVs on PS-MP-triggered inflammatory and autophagic responses in macrophages. Exposure of RAW264.7 cells and primary mouse peritoneal macrophages to PS-MPs (50 nm, 50-200 μg/mL) activated the TLR4/NF-κB signaling pathway and upregulated the autophagy marker LC3B. Notably, treatment with I-EVs (50 and 100 μg/mL) dose-dependently attenuated PS-MP-induced inflammation by suppressing the MyD88/NF-κB axis and downregulating TNF-α and IL-6 expression. Furthermore, I-EVs significantly reduced LC3B levels and inhibited autophagic activation. Mechanistically, I-EVs competitively hindered PS-MP binding to macrophages, thereby preventing its cellular internalization. Collectively, our findings reveal that host-derived I-EVs mitigate PS-MP-induced macrophage inflammation and autophagy by blocking cellular uptake of PS-MPs and modulating key intracellular signaling pathways. This study not only deepens the understanding of microplastic toxicity but also highlights the potential of exploiting endogenous vesicular systems as a strategic intervention against environmental plastic pollution.
Insights
Host-derived extracellular vesicles (I-EVs) protect against polystyrene microplastic (PS-MP) harm. I-EVs reduce PS-MP-induced inflammation and autophagy in macrophages by blocking microplastic uptake.
Area of Science:
- Environmental Health
- Cell Biology
- Immunology
Background:
- Polystyrene microplastics (PS-MPs) are environmental contaminants accumulating in human tissues.
- PS-MPs trigger inflammation and disrupt cellular balance, particularly in the gut.
- Intestinal epithelial cell-derived extracellular vesicles (I-EVs) are crucial for gut integrity, but their role against PS-MP toxicity is unclear.
Purpose of the Study:
- To investigate the protective effects of host-derived I-EVs against PS-MP-induced inflammation and autophagy in macrophages.
- To elucidate the underlying mechanisms by which I-EVs modulate PS-MP toxicity.
Main Methods:
- Exposure of RAW264.7 cells and primary mouse macrophages to PS-MPs (50 nm).
- Treatment with I-EVs (50 and 100 μg/mL) to assess effects on inflammatory and autophagic markers.
- Analysis of signaling pathways including TLR4/NF-κB and MyD88/NF-κB, and cytokine expression (TNF-α, IL-6).
- Evaluation of autophagic marker LC3B levels and PS-MP cellular internalization.
Main Results:
- PS-MPs activated the TLR4/NF-κB pathway and upregulated LC3B, indicating inflammation and autophagy.
- I-EVs dose-dependently reduced PS-MP-induced inflammation by suppressing the MyD88/NF-κB axis and lowering TNF-α and IL-6.
- I-EVs inhibited autophagic activation by reducing LC3B levels.
- I-EVs blocked PS-MP binding to macrophages, preventing cellular uptake.
Conclusions:
- Host-derived I-EVs mitigate PS-MP-induced inflammation and autophagy in macrophages.
- I-EVs exert protective effects by hindering PS-MP cellular internalization and modulating key signaling pathways.
- This highlights the potential of endogenous vesicular systems for combating microplastic pollution effects.
