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Published on: February 28, 2017
Mouse strain-dependent osteoclastogenesis in response to lipopolysaccharide
Ho Gil Choi1, Jin Moon Kim, Bong-Ju Kim
1Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry, Seoul, Republic of Korea.
Journal of Microbiology (Seoul, Korea)
|January 8, 2008
Summary
Bacterial lipopolysaccharide (LPS) differently stimulates osteoclast formation in ddY and ICR mouse strains, with osteoblasts, not preosteoclasts, driving this variation. This highlights the importance of mouse strain selection in osteoclast differentiation research.
Area of Science:
- Cell Biology
- Immunology
- Bone Biology
Background:
- Bacterial lipopolysaccharide (LPS) triggers bone resorption in periodontitis.
- Osteoclast differentiation is crucial for bone remodeling and pathological bone loss.
Purpose of the Study:
- To investigate the differential response of ddY and ICR mouse strains to LPS-induced osteoclastogenesis.
- To determine whether osteoblasts or preosteoclasts are responsible for strain-specific responses to LPS.
Main Methods:
- Co-culture systems of osteoblasts and preosteoclasts from ddY and ICR mice were established.
- Reciprocal co-cultures were performed between the two mouse strains.
- Cells were treated with LPS and 1alpha,25(OH)2D3 to assess osteoclast differentiation.
Main Results:
- Both ddY and ICR mouse strains responded similarly to 1alpha,25(OH)2D3.
- Significant differences in osteoclast differentiation were observed between the strains when stimulated with LPS.
- Reciprocal co-culture experiments indicated that osteoblasts, not preosteoclasts, were responsible for the strain-dependent response to LPS.
Conclusions:
- Osteoblasts from ddY and ICR mice exhibit distinct capacities for mediating LPS-induced osteoclastogenesis.
- The osteoblast is the primary cell type responsible for mouse strain-dependent osteoclastogenesis in response to LPS.
- Caution is advised when using ddY and ICR mouse strains interchangeably for studying osteoclast differentiation and periodontitis models.
