文献类型：期刊文献

英文题名：Sulfated chitosan mitigates acute lung injury induced bone loss via immunoregulation

作者：Liu, Yongxian[1,2];Ji, Luli[1,2];Zhu, Fuwei[1,2];Yu, Jiaze[1,2];Huang, Dongao[1,2];Cui, Jingyuan[1,3];Wang, Xiaogang[1,2,3];Wang, Jing[1,3,4];Liu, Changsheng[2,3]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]East China Univ Sci & Technol, Engn Res Ctr Biomed Mat, Minist Educ, Shanghai, Peoples R China;[3]East China Univ Sci & Technol, Frontiers Sci Ctr Materiobiol & Dynam Chem, Shanghai, Peoples R China;[4]East China Univ Sci & Technol, Minist Educ, Key Lab Ultrafine Mat, Shanghai, Peoples R China

年份：2026

卷号：14

期号：1

外文期刊名：BONE RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001681249400002)】；

基金：This study was supported by the Key Program of the National Natural Science Foundation of China (32230059), the Basic Science Center Program (T2288102), the Foundation of Frontiers Sciesnce Center for Materiobiology and Dynamic Chemistry (JKVD1211002), the National Natural Science Foundation of China (32401128), the Postdoctoral Fellowship Program of CPSF (GZC20230793) and Shanghai Post-doctoral Excellence Program (2023251). We greatly thank Han guo from the Shanghai Synchrotron Radiation Facility BL13HB, for the technical support and assitance in data collection and analysis. We thank the staff members of the Integrated Laser Microscopy System at the National Facility for Protein Science in Shanghai, for providing technical support.

语种：英文

摘要：Respiratory inflammatory diseases disrupt bone metabolism and cause pathological bone loss. The lung-bone axis is established in chronic diseases like asthma and cystic fibrosis but is less studied in acute lung injury (ALI), recently implicated in COVID-19-induced bone loss. This study examined the effects of LPS-induced ALI on bone phenotype and explored the role of 2-N, 6-O sulfated chitosan (26SCS) in mitigating pneumonia-induced bone loss via inflammatory response modulation. Our findings show that 26SCS effectively reaches bone tissue after oral administration. It promotes macrophage polarization to the M2 phenotype, alleviating immune cascade reactions and inhibiting osteoclast-mediated bone resorption. Increased M2 macrophages support type H vessel formation, enhancing inflammatory bone vascularization. These effects foster a favorable osteogenic microenvironment and mitigate ALI-induced bone loss. While dexamethasone is effective in reducing inflammation, it can aggravate ALI-induced bone loss. Our research offers a therapeutic strategy targeting the lung-bone axis for inflammation-induced bone loss.