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Abstract:
This study confirmed that acute lung injury leads to bone loss. It was demonstrated that 2-N, 6-O sulfated chondroitin sulfate can improve bone metabolism disorders related to acute lung injury through immune regulation and alleviate bone loss. It also revealed the differences in intervention effects between this substance and dexamethasone, providing experimental support for the study of bone metabolism abnormalities associated with the lung-bone axis.
01 Research Background
Respiratory inflammatory diseases interfere with bone metabolism and cause pathological bone loss. The lung-bone axis association has been verified in some chronic respiratory diseases. The association between acute lung injury and bone loss is insufficiently studied. This acute lung disease has also been found to be related to bone loss caused by specific viral infections.
02 Main Content
Using lipopolysaccharide-induced acute lung injury as a model, the impact on bone phenotype was analyzed; the role and mechanism of 2-N, 6-O sulfated chondroitin sulfate in improving bone loss induced by pneumonia through regulating inflammatory responses were explored; the differences in intervention effects between this substance and dexamethasone in acute lung injury and related bone loss were compared.
03 Research Design
An acute lung injury experimental model induced by lipopolysaccharide was constructed, and the 2-N, 6-O sulfated chondroitin sulfate intervention group and the dexamethasone control group were set up. The distribution of the tested substances in bone tissue, macrophage polarization, immune response, osteoclast activity, bone vascularization, and bone phenotype were detected.
04 Results
2-N, 6-O sulfated chondroitin sulfate can effectively reach bone tissue after oral administration; this substance can promote macrophage polarization to the M2 phenotype, alleviate the immune cascade reaction, and inhibit bone resorption mediated by osteoclasts; the increase of M2-type macrophages can support H-type vascular formation, improve the bone vascularization level in the inflammatory state, construct a microenvironment conducive to bone formation, and alleviate bone loss caused by acute lung injury; dexamethasone can reduce inflammation but will aggravate bone loss related to acute lung injury.
05 Extension of Thoughts
Based on the lung-bone axis regulatory mechanism, further explore targeted intervention substances for inflammation-related bone loss; expand the research on the immune regulatory and bone metabolism regulatory effects of sulfated polysaccharides in other inflammatory-associated bone metabolism abnormal diseases; deeply analyze the intrinsic relationship between macrophage polarization, bone vascularization, and bone metabolism, and improve the lung-bone axis regulatory network.
Original Source:
1. Journal: Bone Research
2. Publication Date: 2026-02-05
3. DOI: 10.1038/s41413-025-00475-4
4. Authors: Yongxian Liu, Luli Ji, Fuwei Zhu, Jiaze Yu, Dongao Huang, Jingyuan Cui, Xiaogang Wang, Jing Wang, Changsheng Liu
