宿主来源的肠细胞外小泡抑制聚苯乙烯微塑料诱导的巨噬细胞炎症和自噬的激活
Host-Derived Intestinal Extracellular Vesicles Inhibit Polystyrene Microplastic-Induced Activation of Inflammation and Autophagy in Macrophages.
摘要(中文译文)
聚苯乙烯微塑料（PS-MPs）作为普遍存在的环境污染物，主要通过食物链进入人体并在肠道组织中蓄积，引发炎症反应并破坏细胞稳态。尽管肠上皮细胞来源的细胞外囊泡（I-EVs）在维持肠道完整性方面的调控作用已被认可，但其对PS-MPs诱导的肠道炎症和自噬的潜在保护作用仍知之甚少。本研究探讨了宿主来源的I-EVs对PS-MPs触发的巨噬细胞炎症和自噬反应的影响。将RAW264.7细胞和原代小鼠腹腔巨噬细胞暴露于PS-MPs（50 nm，50-200 μg/mL）后，TLR4/NF-κB信号通路被激活，自噬标志物LC3B表达上调。值得注意的是，I-EVs（50和100 μg/mL）处理可剂量依赖性地减轻PS-MPs诱导的炎症，其机制为抑制MyD88/NF-κB轴并下调TNF-α和IL-6的表达。此外，I-EVs显著降低了LC3B水平并抑制了自噬激活。在机制上，I-EVs竞争性阻碍PS-MPs与巨噬细胞的结合，从而阻止其被细胞内化。综上所述，本研究发现宿主来源的I-EVs通过阻断巨噬细胞对PS-MPs的摄取并调节关键细胞内信号通路，减轻PS-MPs诱导的巨噬细胞炎症和自噬。本研究不仅加深了对微塑料毒性的认识，还凸显了利用内源性囊泡系统作为应对环境塑料污染的策略性干预手段的潜力。
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.
如何引用
AMA
Runze Wang, Chaoqiao Wang, Binjin Hu, Qiuyu Zhang, Jixin Xu, Yiting Huang, et al. Host-Derived Intestinal Extracellular Vesicles Inhibit Polystyrene Microplastic-Induced Activation of Inflammation and Autophagy in Macrophages.. ACS applied materials & interfaces. 2026; doi:10.1021/acsami.6c02042.
APA
Runze Wang, Chaoqiao Wang, Binjin Hu, Qiuyu Zhang, Jixin Xu, Yiting Huang, et al (2026). Host-Derived Intestinal Extracellular Vesicles Inhibit Polystyrene Microplastic-Induced Activation of Inflammation and Autophagy in Macrophages.. ACS applied materials & interfaces. https://doi.org/10.1021/acsami.6c02042
GB/T 7714
Runze Wang, Chaoqiao Wang, Binjin Hu, Qiuyu Zhang, Jixin Xu, Yiting Huang, et al. Host-Derived Intestinal Extracellular Vesicles Inhibit Polystyrene Microplastic-Induced Activation of Inflammation and Autophagy in Macrophages.[J]. ACS applied materials & interfaces, 2026 doi:10.1021/acsami.6c02042.
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