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Updated: Mar 9, 2026
Isolation, Purification and Labeling of Mouse Bone Marrow Neutrophils for Functional Studies and Adoptive Transfer Experiments
Published on: July 10, 2013
Data on the NADPH-oxidase activity induced by WKYMVm and galectin-3 in bone marrow derived and exudated neutrophils
Lena Björkman1, Huamei Forsman1, Karin Önnheim1
1Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Sweden.
Abstract:
Neutrophils are the key players in inflammatory reactions and the release of superoxide through the NADPH-oxidase upon neutrophil activation contributes to bacterial clearance and surrounding tissue damage. Here we describe data on the mouse neutrophil NADPH-oxidase activation induced by the mouse formyl peptide receptor (Fpr) agonist WKYMVm and galectin-3. Neutrophils isolated from bone marrow, peritoneal exudated, and in vitro TNFα primed bone marrow neutrophils from four different laboratory strains (C57BL/6, DBA/1, BALB/c and NMRI) were used. Both Fpr agonist and galectin-3 activated neutrophils to release superoxide. No differences were observed in the amounts of superoxide released from neutrophils derived from four different strains.
Insights
Neutrophil activation by formyl peptide receptor agonists and galectin-3 triggers superoxide release. This study found no significant differences in superoxide release among neutrophils from four different mouse strains, indicating conserved responses.
Area of Science:
- Immunology
- Cell Biology
- Inflammation Research
Background:
- Neutrophils are critical immune cells involved in inflammation and host defense.
- Neutrophil activation leads to the release of superoxide via NADPH oxidase, crucial for pathogen killing but also implicated in tissue damage.
- Understanding neutrophil activation pathways is key to modulating inflammatory responses.
Purpose of the Study:
- To investigate mouse neutrophil NADPH oxidase activation.
- To assess the role of formyl peptide receptor (Fpr) agonists and galectin-3 in neutrophil activation.
- To compare superoxide release from neutrophils across different mouse strains.
Main Methods:
- Isolation of neutrophils from mouse bone marrow and peritoneal exudates.
- In vitro TNFα priming of bone marrow neutrophils.
- Stimulation of neutrophils with an Fpr agonist (WKYMVm) and galectin-3.
- Measurement of superoxide release using four common laboratory mouse strains (C57BL/6, DBA/1, BALB/c, NMRI).
Main Results:
- Both the Fpr agonist WKYMVm and galectin-3 effectively activated mouse neutrophils to release superoxide.
- Neutrophils isolated from bone marrow, peritoneal exudates, and TNFα-primed bone marrow neutrophils all exhibited activation.
- No significant strain-dependent differences were observed in the quantity of superoxide released by neutrophils from the four tested mouse strains.
Conclusions:
- Mouse formyl peptide receptor agonists and galectin-3 are potent activators of neutrophil superoxide production.
- Neutrophil responses to these stimuli are consistent across commonly used laboratory mouse strains.
- These findings provide a baseline for further studies on neutrophil function and inflammatory mechanisms in different genetic backgrounds.
