Related Experiment Video
Updated: Aug 8, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Role of type I interferons during macrophage activation by lipopolysaccharide
P K Vadiveloo1, G Vairo, P Hertzog
1The Bernard O'Brien Institute of Microsurgery, Fitzroy, 3065, Australia. vadivep@svhm.org.au
Insights
Type I interferons (IFNs) are crucial for macrophage nitric oxide production stimulated by lipopolysaccharide (LPS). However, type I IFNs also inhibit respiratory burst and mediate anti-proliferative effects, showing diverse roles in macrophage responses.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophages are key immune cells activated by bacterial lipopolysaccharide (LPS).
- Type I interferons (IFNs) are secreted during LPS activation and can act on the same cell (autocrine).
Purpose of the Study:
- To investigate the specific roles of type I IFNs in macrophage responses to LPS.
- To elucidate the mechanisms by which type I IFNs modulate macrophage functions.
Main Methods:
- Utilized bone marrow-derived macrophages (BMM) from IFNAR1-/- mice, which lack type I IFN receptor signaling.
- Compared responses of IFNAR1-/- BMM to wild-type (WT) BMM upon LPS stimulation.
- Assessed nitric oxide (NO) production, inducible NO synthase (iNOS) expression, respiratory burst activity, proliferation, and apoptosis.
Main Results:
- Type I IFNs are essential for LPS-induced nitric oxide (NO) production and inducible NO synthase (iNOS) expression in BMM.
- Type II IFN (IFN-gamma) could rescue NO production in IFNAR1-/- BMM.
- Type I IFNs negatively regulate respiratory burst activity in LPS-primed BMM.
- Type I IFNs mediate the anti-proliferative effects of low LPS concentrations, but higher LPS concentrations act independently of type I IFNs.
- Type I IFNs promote BMM survival, yet LPS-induced anti-apoptosis is independent of type I IFNs.
Conclusions:
- Type I IFNs play multifaceted roles in LPS-stimulated macrophage responses, being essential for NO production but inhibitory for respiratory burst.
- These findings reveal complex regulatory functions of type I IFNs in innate immunity and macrophage activation.
Abstract:
Activation of macrophages by bacterial lipopolysaccharide (LPS) is accompanied by the secretion of type I interferons (IFNs) which can act in an autocrine manner. We examined the role of type I IFNs in macrophage responses to LPS using bone marrow-derived macrophages (BMM) from IFNAR1-/- mice, which lack a component of the type I IFN receptor and do not respond to type I IFNs. We found that, unlike wild-type (WT) BMM, LPS-treated IFNAR1-/- cells failed to produce nitric oxide (NO), or express inducible NO synthase (iNOS), indicating that type I IFNs are essential for all LPS-stimulated NO production in BMM. Exogenously added type II IFN (IFNgamma) rescued these responses in LPS-treated IFNAR1-/- BMM. In contrast to effects on NO, type I IFNs negatively regulated respiratory burst activity in LPS-primed BMM. We also found that while type I IFNs mediated the anti-proliferative effects of lower concentrations of LPS, at higher concentrations LPS acted in a type I IFNs-independent manner. Finally, we report that type I IFNs are a survival factor for BMM. Despite this, the ability of LPS to also prevent apoptosis in BMM was independent of type I IFNs. These findings highlight the diverse roles of type I IFNs in mediating LPS-stimulated macrophage responses.
More Related Videos
Related Concept Videos
Cell-mediated Immune Responses
Immune Surveillance by NK Cells and Phagocytes
Natural Killer Cells: The Fast Responders
NK cells are large granular lymphocytes found in the blood and lymphatic system. These...
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Immune Response Against Viral Pathogens
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Formation of Lipopolysaccharides
Type I Diabetes II: Pathophysiology

