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Aging-induced decrease in progenitor B cells enhances the osteoclastogenesis of bone marrow macrophages via

Ruiqing Sun1, Lan Luo1, Yang Chen1

  • 1Department of Pediatric Dentistry, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices& Beijing Key Laboratory of Digital Stomatology & NHC Key Laboratory of Digital Stomatology & NMPA Key Laboratory for Dental Materials, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, P.R. China.

Immunity & Ageing : I & A
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PubMed
Summary
This summary is machine-generated.

Oxidative stress in senile osteoporosis accelerates B lymphocyte immune-senescence, reducing progenitor B cells. This activates a pathway promoting bone-resorbing osteoclast formation, suggesting CCR1 antagonists as a therapeutic target.

Keywords:
Fos/CCL3 signaling‌ pathwayImmune-senescenceMacrophageProgenitor B cellsROSSenile osteoporosis

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Area of Science:

  • Immunology
  • Bone Biology
  • Gerontology

Background:

  • Senile osteoporosis (SOP) poses a significant health challenge due to increased fracture risk in the elderly.
  • The precise role of immune cell changes in SOP pathogenesis remains largely undefined.

Purpose of the Study:

  • To elucidate the mechanistic link between immune cell alterations and senile osteoporosis.
  • To investigate the impact of oxidative stress on immune cells within the bone marrow microenvironment in SOP.

Main Methods:

  • Utilized senescence-accelerated mouse prone 6 (SAMP6) mice as an SOP model, compared to senescence-accelerated mouse resistant 1 (SAMR1) controls.
  • Employed multi-omics (single-cell RNA sequencing, transcriptomics), flow cytometry, and histological analyses to study bone marrow immune cells.
  • Investigated cell interactions and osteoclastogenesis in vitro, using a CCR1 antagonist (BX471) to block specific pathways.

Main Results:

  • SAMP6 mice exhibited reduced bone mass and elevated reactive oxygen species (ROS).
  • A significant depletion of B lymphocytes, particularly pro-B cells, was observed in SAMP6 mice.
  • Oxidative stress induced the Fos/Ccl3 axis in pro-B cells, promoting osteoclastogenesis via the CCL3-CCR1 axis, an effect suppressed by BX471.

Conclusions:

  • Elevated ROS accelerates B lymphocyte immune-senescence in SOP, reducing progenitor B cells.
  • This process activates the Fos/Jun pathway, leading to CCL3 overexpression and enhanced macrophage osteoclastogenesis.
  • Targeting the CCL3-CCR1 axis with antagonists offers a potential therapeutic strategy for senile osteoporosis.