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Updated: Jul 14, 2026
09:57
Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Thermal injury elevates the inflammatory monocyte subpopulation in multiple compartments.
John G Noel1, Andrew Osterburg, Quan Wang
1Shriners Hospital for Children, 3229 Burnet Avenue, Cincinnati, OH 45229, USA. gnoel@shrinenet.org
Shock (Augusta, Ga.)
|July 4, 2007
Summary
Following thermal injury, inflammatory monocytes (IMs) significantly increase in mice, becoming a primary source of TNF-alpha. This study investigates monocyte changes and their role in the burn injury response.
Area of Science:
- Immunology
- Wound Healing
- Cell Biology
Background:
- Human resident and inflammatory monocyte (IM) subpopulations have rodent equivalents.
- The impact of thermal injury on these monocyte subpopulations remains unstudied.
Purpose of the Study:
- To investigate the effect of thermal injury on resident and inflammatory monocyte subpopulations in mice.
- To determine the role of inflammatory monocytes in TNF-alpha production and lymphocyte proliferation post-burn.
Main Methods:
- Mice were subjected to scald burns and euthanized on postburn days 2, 4, and 8.
- Monocyte subpopulations (resident monocytes, IMs) and progenitors (macrophage-colony-forming units [M-CFU]) were quantified in bone marrow, blood, and spleen.
- TNF-alpha production and lymphocyte proliferation inhibition by monocyte fractions were assessed.
Main Results:
- A significant increase in IMs was observed across all compartments by postburn day 8.
- Macrophage-colony-forming units (M-CFU) increased in blood and spleen, with a non-significant trend in bone marrow.
- Inflammatory monocytes (IMs) were identified as a major source of TNF-alpha in all compartments post-burn.
Conclusions:
- Thermal injury leads to a significant expansion of inflammatory monocytes (IMs) in mice.
- Inflammatory monocytes (IMs) are a key source of TNF-alpha following burn injury.
- The observed increase in splenic monocyte progenitors and IMs correlates with chemokine expression.
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