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Specifc inflammatory osteoclast precursors induced during chronic inflammation give rise to highly active osteoclasts associated with inflammatory bone loss

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Bone Research 2022年第3期10卷 548-564页

作者： Yaron Meirow Milena Jovanovic Yuval Zur Juliana Habib Daniele Filippo Colombo Nira Twaik Hadas Ashkenazi-Preiser Kerem Ben-Meir Ivan Mikula Jr. Or Reuven Guy Kariv Leonor Daniel Saja Baraghithy Yehuda Klein Jeroen Krijgsveld Noam Levaot michal baniyash The Concern Foundation Laboratories at The Lautenberg Center for Immunology and Cancer Research Israel-Canada Medical Research InstituteFaculty of MedicineThe Hebrew UniversityJerusalemIsrael Department of Physiology and Cell Biology Ben-Gurion University of the NegevBeer-ShevaIsrael Division of Proteomics of Stem Cells and Cancer German Cancer Research Center(DKFZ)HeidelbergGermany Institute for Drug Research Faculty of MedicineThe Hebrew UniversityJerusalemIsrael Hebrew University-Hadassah School of Dental Medicine JerusalemIsrael Heidelberg University Medical FacultyHeidelbergGermany

Elevated osteoclast(OC)activity is a major contributor to inflammatory bone loss(IBL)during chronic inflammatory ***,the specific OC precursors(OCPs)responding to inflammatory cues and the underlying mechanisms leading to IBL are poorly *** identified two distinct OCP subsets:Ly6C^(hi)CD11b^(hi) inflammatory OCPs(iOCPs)induced during chronic inflammation,and homeostatic Ly6C^(hi)CD11b^(lo)OCPs(hOCPs)which remained *** and proteomic characterization revealed that while iOCPs were rare and displayed low osteoclastogenic potential under normal conditions,they expanded during chronic inflammation and generated OCs with enhanced *** contrast,hOCPs were abundant and manifested high osteoclastogenic potential under normal conditions but generated OCs with low activity and were unresponsive to the inflammatory *** derived from iOCPs expressed higher levels of resorptive and metabolic proteins than those generated from hOCPs,highlighting that different osteoclast populations are formed by distinct *** further identified the TNF-αand S100A8/A9 proteins as key regulators that control the iOCP response during chronic ***,we demonstrated that the response of iOCPs but not that of hOCPs was abrogated in tnf-α^(-/-)mice,in correlation with attenuated *** findings suggest a central role for iOCPs in IBL *** can serve as potential biomarkers for IBL detection and possibly as new therapeutic targets to combat IBL in a wide range of inflammatory conditions.

关键词： inflammation inflammatory osteoclast

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