Research Paper Volume 16, Issue 6 pp 5703—5710
M1 intestinal macrophages-derived exosomes promote colitis progression and mucosal barrier injury
- 1 College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China
- 2 Department of Pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314001, China
- 3 Department of Cardiology, Shenyang Medical College Affiliated Second Hospital, Shenyang 314005, China
Received: September 28, 2023 Accepted: December 7, 2023 Published: March 26, 2024
https://doi.org/10.18632/aging.205672How to Cite
Copyright: © 2024 Du et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Aim: This work aimed to investigate the role of M1 intestinal macrophages-derived exosomes (M1-Exo) in colitis and its mechanism.
Methods: M1 polarization of intestinal macrophages was induced in vitro, and their exosomes were extracted and identified. Thereafter, the DSS-induced colitis mouse model was built. Each mouse was given intraperitoneal injection of exosomes, and then mouse weight and DAI were dynamically monitored. In addition, the levels of cytokines were detected by ELISA. After treatment with the TLR4 inhibitor Resatorvid, the effects of M1 macrophages-derived exosomes were observed. Besides, the mouse intestinal epithelial cells were cultured in vitro for observing function of M1-Exo.
Results: M1-exo aggravated the colitis and tissue inflammation in mice, activated the TLR4 signal, and destroyed the mucosal barrier. But M0 macrophages-derived exosomes (M0-Exo) did not have the above effects. Resatorvid treatment antagonized the roles of M1-exo. Moreover, as confirmed by cellular experiments in vitro, M1-exo destroyed mucosal barrier.
Conclusion: M1-exo serve as the pro-inflammatory mediator, which can promote mouse colitis progression by activating TLR4 signal.