文献类型：期刊文献

中文题名：Sulfated chitosan mitigates acute lung injury induced bone lossvia immunoregulation

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

机构：[1]The State Key Laboratory of Bioreactor Engineering,East China University of Science and Technology,Shanghai,China;[2]Engineering Research Center for Biomedical Materials of the Ministry of Education,East China University of Science and Technology,Shanghai,China;[3]Frontiers Science Center for Materiobiology and Dynamic Chemistry,East China University of Science and Technology,Shanghai,China;[4]Key Laboratory for Ultrafine Materials of Ministry of Education,East China University of Science and Technology,Shanghai,China

年份：2026

卷号：14

期号：1

起止页码：166

中文期刊名：Bone Research

外文期刊名：骨研究(英文版)

基金：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);Shanghai Post-doctoral Excellence Program(2023251)。

语种：英文

中文关键词：bone phenotype;bone metabolism;chronic diseases;inflammatory response modulationour;respiratory inflammatory diseases;cystic fibrosis;sulfated chitosan;acute lung injury;

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.