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Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model
Published on: April 24, 2020
Cross-Tissue Transcriptomic Convergence Identifies a Leuko-Cyte-Shared, Myeloid-Enriched Inflammatory Program in
Wang Wei1, Bingxiao Pan1, Ruiying Li1
1Department of Sports Medicine and Pediatric Orthopaedics, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an Jiaotong University, No. 157, Xiwu Road, Xi'an 710004, China.
International Journal of Molecular Sciences
|August 13, 2026
Summary
Frailty and osteoarthritis share an inflammatory molecular program, primarily involving myeloid cells across tissues. This finding offers a new framework for understanding these common conditions in older adults.
Area of Science:
- Gerontology
- Immunology
- Molecular Biology
Background:
- Frailty and osteoarthritis (OA) are common in older adults and may share underlying molecular mechanisms.
- The extent of shared molecular programs across different tissues in frailty and OA is not well understood.
Purpose of the Study:
- To investigate shared molecular programs between frailty and osteoarthritis across multiple tissue types.
- To identify specific cellular players and signaling pathways involved in the convergence of frailty and OA.
Main Methods:
- Integrated bulk transcriptomics, peripheral immune, and OA meniscal single-cell atlases.
- Performed cell-cell communication inference and in vitro myeloid-chondrocyte co-culture models.
- Utilized protein-protein interaction analysis and donor-aware pseudobulk analysis.
Main Results:
- Identified a 16-gene inflammatory and migratory program shared between frailty-associated vastus lateralis and OA synovium, refined to a 15-gene hub module (Hub-15).
- Observed coordinated Hub-15 upregulation in various leukocyte populations, particularly monocytes/macrophages, in frailty and OA.
- Found altered proportions of inflammatory/stress and fibrochondrocyte-like cells in OA menisci, but no significant state-specific Hub-15 differences after correction.
Conclusions:
- A cross-tissue, leukocyte-shared, and myeloid-enriched inflammatory program converges in independent frailty and OA cohorts.
- This shared program provides a hypothesis-generating framework for future mechanistic studies of frailty and OA.
- In vitro models confirmed that myeloid-derived factors can induce inflammatory and matrix-catabolic responses in chondrocytes.