STING/Type I Interferon Pathway Activation Confers Multimodal Therapeutic Benefits in Osteomyelitis
6 affiliations
- 1Department of Orthopedic Surgery National Regional Medical Center Binhai Campus of the First Affiliated Hospital Fujian Medical University Fuzhou China
- 2Department of Orthopedic Surgery The First Affiliated Hospital of Fujian Medical University Fuzhou China
- 3Fujian Provincial Institute of Orthopedics, the First Affiliated Hospital Fujian Medical University Fuzhou China
- 4Department of Orthopedic Surgery Affiliated Hospital of Putian University Putian China
- 5Key Laboratory of Orthopedics & Traumatology of Traditional Chinese Medicine and Rehabilitation Ministry of Education Fujian University of Traditional Chinese Medicine Fuzhou China
- 6Department of Laboratory Medicine The First Affiliated Hospital of Fujian Medical University Fuzhou China
Abstract
Osteomyelitis is an inflammatory bone disease caused by pathogenic microorganisms and characterized by severe pain, extensive bone destruction, and reduced antibiotic efficacy due to local abscess formation. This study investigates the therapeutic potential of activating the STING (stimulator of interferon genes) pathway in osteomyelitis. In murine femoral osteomyelitis models induced by Staphylococcus aureus (S. aureus), STING agonists alleviate osteomyelitis‐associated pain, suppress infection‐induced bone destruction, and reduce local abscess formation. These effects depend on host STING/type I interferon (IFN‐I) signaling and involve three mechanisms: inhibition of nociceptor activation by pathogens, suppression of osteoclast differentiation and function without affecting osteoblast activity, and downregulation of interleukin‐1β (IL‐1β), leading to reduced neutrophil recruitment and abscess formation. By reducing abscess formation as a physical barrier, STING agonists enhance the antibacterial efficacy of conventional antibiotics such as vancomycin at the site of infection. In summary, these findings suggest that the synergistic mechanisms activated by STING represent a promising therapeutic target for alleviating pain and improving clinical outcomes in osteomyelitis.
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BibTeX
@article{chen2026stingtype,
title = {{STING/Type I Interferon Pathway Activation Confers Multimodal Therapeutic Benefits in Osteomyelitis}},
author = {Yang Chen and Jianhua Lv and Yuanqing Cai and Xuhui Yuan and Hongxin Hu and Jiayu Li and Yiming Lin and Hongyan Li and Lan Lin and Huangfeng Lin and Chaofan Zhang and Qijin Wang and Ying Huang and Zida Huang and Wenbo Li and Susheng Niu and Jianhua Lin and Bin Yang and Xinyu Fang and Wenming Zhang},
journal = {Advanced Science},
year = {2026},
month = oct,
doi = {10.1002/advs.77892},
url = {https://doi.org/10.1002/advs.77892},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - STING/Type I Interferon Pathway Activation Confers Multimodal Therapeutic Benefits in Osteomyelitis
AU - Yang Chen
AU - Jianhua Lv
AU - Yuanqing Cai
AU - Xuhui Yuan
AU - Hongxin Hu
AU - Jiayu Li
AU - Yiming Lin
AU - Hongyan Li
AU - Lan Lin
AU - Huangfeng Lin
AU - Chaofan Zhang
AU - Qijin Wang
AU - Ying Huang
AU - Zida Huang
AU - Wenbo Li
AU - Susheng Niu
AU - Jianhua Lin
AU - Bin Yang
AU - Xinyu Fang
AU - Wenming Zhang
PY - 2026
DA - 2026/10/26
JO - Advanced Science
DO - 10.1002/advs.77892
UR - https://doi.org/10.1002/advs.77892
AB - Osteomyelitis is an inflammatory bone disease caused by pathogenic microorganisms and characterized by severe pain, extensive bone destruction, and reduced antibiotic efficacy due to local abscess formation. This study investigates the therapeutic potential of activating the STING (stimulator of interferon genes) pathway in osteomyelitis. In murine femoral osteomyelitis models induced by Staphylococcus aureus (S. aureus), STING agonists alleviate osteomyelitis‐associated pain, suppress infection‐induced bone destruction, and reduce local abscess formation. These effects depend on host STING/type I interferon (IFN‐I) signaling and involve three mechanisms: inhibition of nociceptor activation by pathogens, suppression of osteoclast differentiation and function without affecting osteoblast activity, and downregulation of interleukin‐1β (IL‐1β), leading to reduced neutrophil recruitment and abscess formation. By reducing abscess formation as a physical barrier, STING agonists enhance the antibacterial efficacy of conventional antibiotics such as vancomycin at the site of infection. In summary, these findings suggest that the synergistic mechanisms activated by STING represent a promising therapeutic target for alleviating pain and improving clinical outcomes in osteomyelitis.
SN - 2198-3844
ER -