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Proteomic Analysis of Human Macrophage Polarization Under a Low Oxygen Environment
Published on: January 7, 2019
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Transcriptomic profiling reveals a dramatic inflammatory shift in osteal macrophages during colitis-induced
Ryota Suzuki1, Liyile Chen1, Tsutomu Endo1
1Department of Orthopedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita-15, Nish-7, Kita-ku, Sapporo, 060-8638, Japan.
Summary
Colitis causes bone loss by altering osteal macrophages (Omacs). These immune cells become inflammatory, disrupting bone metabolism and leading to osteoporosis.
Area of Science:
- Immunology
- Bone Biology
- Gastroenterology
Background:
- Colitis compromises the intestinal barrier, allowing microbial products to reach distant organs like bone.
- Macrophages in bone (Omacs) are crucial for bone homeostasis and immune defense.
Purpose of the Study:
- Investigate molecular changes in Omacs during colitis.
- Determine Omacs' role in colitis-induced bone loss and osteoporosis.
Main Methods:
- Induced colitis in mice using DSS (dextran sulfate sodium).
- Isolated Omacs for bulk RNA-sequencing, phagocytosis assays, and co-culture studies.
- Assessed Omac interactions with osteoblasts and osteoclast precursors.
Main Results:
- Colitis induced an inflammatory Omac phenotype, correlating with bone loss.
- Upregulated inflammatory pathways in Omacs included IL-17, NF-κB, and TNF signaling.
- Omacs showed reduced phagocytosis and impaired osteoblast/osteoclast differentiation.
Conclusions:
- Colitis triggers Omac inflammation, contributing to bone metabolic dysfunction.
- Targeting inflammatory pathways in Omacs may treat colitis-induced osteoporosis.
