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急性肺损伤小鼠中外泌体分泌的调控

Exosome Secretion Regulation in Mice with Acute Lung Injury.

作者信息

Jie Hui-Hui, Lu Wei-Hua

机构信息

Department of Critical Care Medicine, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, Anhui, 241001, People's Republic of China.

Graduate School of Wannan Medical University, Wuhu, Anhui, 241001, People's Republic of China.

出版信息

J Inflamm Res. 2025 Jun 3;18:7151-7165. doi: 10.2147/JIR.S506693. eCollection 2025.

DOI:10.2147/JIR.S506693
PMID:40487284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12145097/
Abstract

PURPOSE

Acute lung injury (ALI) is a typical critical illness. Exosomes can regulate the development of pulmonary inflammation by modulating macrophage metabolism and behavior. During ALI, C-C motif chemokine ligand 2 (CCL2) is involved in the occurrence and maintenance of the inflammatory response, and the amount of CCL2 secreted by exosome increases. This study was aimed at investigating the role and mechanism of exosome -mediated CCL2 in sepsis-related ALI using a sepsis model in mice and rat type II alveolar epithelial cells. Furthermore, we explore the regulation of extracellular vesicle secretion in acute lung injury in mice.

METHODS

The sepsis group was pretreated with an exosome inhibitor to determine the extent of exosome release and alterations in inflammatory factors in the lung tissue. Furthermore, RLE-6TN cell-derived exosomes were cocultured with rat alveolar macrophages. Subsequently, an ALI rat model was constructed, and exosomes produced in vitro were injected into rats via the tail vein to detect the expression levels of inflammatory factors and elucidate macrophage polarization pathways.

RESULTS

After treatment with the exosome inhibitor, the number of exosomes and the expression of CCL2 in the lung tissue were significantly downregulated in the sepsis group. Exosomes secreted by lipopolysaccharide-treated rat type II alveolar epithelial cells stimulated the polarization of M1 macrophages, which resulted in morphological and functional changes.

CONCLUSION

Exosome Secretion Regulation in Mice with Acute Lung Injury.

摘要

目的

急性肺损伤（ALI）是一种典型的危重病。外泌体可通过调节巨噬细胞代谢和行为来调控肺部炎症的发展。在ALI期间，C-C基序趋化因子配体2（CCL2）参与炎症反应的发生和维持，且外泌体分泌的CCL2量增加。本研究旨在利用小鼠脓毒症模型和大鼠II型肺泡上皮细胞，探讨外泌体介导的CCL2在脓毒症相关ALI中的作用及机制。此外，我们还探究了小鼠急性肺损伤中细胞外囊泡分泌的调控情况。

方法

脓毒症组用外泌体抑制剂预处理，以确定外泌体释放程度及肺组织中炎症因子的变化。此外，将RLE-6TN细胞来源的外泌体与大鼠肺泡巨噬细胞共培养。随后，构建ALI大鼠模型，并通过尾静脉将体外产生的外泌体注入大鼠体内，以检测炎症因子的表达水平并阐明巨噬细胞极化途径。

结果

脓毒症组用外泌体抑制剂处理后，肺组织中外泌体数量及CCL2表达均显著下调。脂多糖处理的大鼠II型肺泡上皮细胞分泌的外泌体刺激M1巨噬细胞极化，导致其形态和功能发生变化。

结论

急性肺损伤小鼠的外泌体分泌调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/cc4bcb39768c/JIR-18-7151-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/2281f4f17369/JIR-18-7151-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/b26c3d0d817a/JIR-18-7151-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/95e8f03c45c1/JIR-18-7151-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/2ba0f333e422/JIR-18-7151-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/9d6f9c0a2382/JIR-18-7151-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/3a7e7515439f/JIR-18-7151-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/6ed5aab2a3f2/JIR-18-7151-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/cc4bcb39768c/JIR-18-7151-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/2281f4f17369/JIR-18-7151-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/b26c3d0d817a/JIR-18-7151-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/95e8f03c45c1/JIR-18-7151-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/2ba0f333e422/JIR-18-7151-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/9d6f9c0a2382/JIR-18-7151-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/3a7e7515439f/JIR-18-7151-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/6ed5aab2a3f2/JIR-18-7151-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce9b/12145097/cc4bcb39768c/JIR-18-7151-g0008.jpg

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