Engineered exosomes with enriched miR-23b suppress the progression of periodontitis by reprogramming macrophages

Tianyuan Qiu; Zengguang Liu; Hugang Zhang; Jiaxin Jia; Xinxin Shao; Sihan Wang; Haobo Han; Quanshun Li; Min Hu

doi:10.1016/j.colsurfb.2025.114947

Engineered exosomes with enriched miR-23b suppress the progression of periodontitis by reprogramming macrophages

Colloids Surf B Biointerfaces. 2025 Jul 11:255:114947. doi: 10.1016/j.colsurfb.2025.114947. Online ahead of print.

Authors

Tianyuan Qiu¹, Zengguang Liu², Hugang Zhang², Jiaxin Jia², Xinxin Shao², Sihan Wang³, Haobo Han⁴, Quanshun Li⁵, Min Hu⁶

Affiliations

¹ Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Department of Orthodontics, Hospital of Stomatology, Jilin University, Changchun 130021, China; Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.
² Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China.
³ Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Department of Orthodontics, Hospital of Stomatology, Jilin University, Changchun 130021, China.
⁴ Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China. Electronic address: hanhaobo@jlu.edu.cn.
⁵ Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, School of Life Sciences, Jilin University, Changchun 130012, China. Electronic address: quanshun@jlu.edu.cn.
⁶ Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Department of Orthodontics, Hospital of Stomatology, Jilin University, Changchun 130021, China. Electronic address: humin@jlu.edu.cn.

PMID: 40652875
DOI: 10.1016/j.colsurfb.2025.114947

Abstract

Periodontitis is a prevalent inflammatory disease that damages the tooth-supporting structure, leading to tooth instability and loss. Conventional therapies target biofilms but fail to address immune dysregulation, highlighting the need of host-modulating strategies. Herein, the decreased miR-23b level was found to be associated with the progression of periodontitis and identified as a potential therapeutic agent for the disease. Since the conventional methods of loading exogenous miRNAs into exosomes may impair the membrane structure, a miR-23b-overexpressed HEK293T cell line was constructed to produce engineered exosomes with enriched miR-23b (namely miR-23b-Exo). The miR-23b-Exo modulated the NF-κB signaling pathway in macrophages, thereby promoting the M2 polarization and suppressing the release of inflammatory cytokines to execute the anti-inflammatory effect. In rats with periodontitis, miR-23b-Exo alleviated the inflammation-induced periodontal damage, exhibiting favorable anti-periodontitis efficacy. Our study provides a promising host-modulating strategy based on the engineered exosomes-mediated miR-23b delivery, thereby alleviating periodontal damage by reprogramming macrophages.

Keywords: Engineered exosomes; Inflammation; MiR-23b; NF-κB signaling pathway; Periodontitis.