Related Experiment Video
Updated: Feb 22, 2026
Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Pentraxin-3 regulates the inflammatory activity of macrophages
Aya Shiraki1, Norihiko Kotooka1, Hiroshi Komoda1
1Department of Cardiovascular Medicine, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga, Japan.
Background And Aims:
Pentraxin-3 (PTX3) reportedly has protective roles in atherosclerosis and myocardial infarction, and is a useful biomarker of vascular inflammation. However, the detailed functions of PTX3 in inflammation are yet to be elucidated. This study aimed to investigate the function of PTX3 in macrophages.
Methods:
PMA-treated THP-1 cell line (THP-1 macrophage) and monocyte-derived human primary macrophages were treated with recombinant PTX3. Cytokine and chemokine levels in the THP-1 culture medium were measured as well as monocyte chemoattractant protein (MCP-1) concentrations in the Raw 264.7 cell culture medium. PTX3-silenced apoptotic macrophages (THP-1 cell line) were generated to investigate the roles of PTX3 in phagocytosis.
Results:
In the presence of PTX3, macrophage interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α) and MCP-1 levels were reduced significantly (-39%, P=0.007; -21%, P=0.008; and -67%, P=0.0003, respectively), whilst activated transforming growth factor-β (TGF-β) was detected in the THP-1 macrophages (P=0.0004). Additionally, PTX3 induced Akt phosphorylation and reduced nuclear factor-kappa B (NF-κB) activation by 35% (P=0.002), which was induced by TNF-α in THP-1 macrophages. Furthermore, silencing of PTX3 in apoptotic cells resulted in increased macrophage binding, elevated expression rate of HLA-DR (+30%, P=0.015) and CD86 (+204%, P=0.004) positive cells, and induction of IL-1β (+36%, P=0.024) production. Conversely, adding recombinant PTX3 to macrophages reduced CD86 and HLA-DR expression in a dose-dependent manner.
Conclusions:
We identified PTX3 as a novel regulator of macrophage activity, and this function suggests that PTX3 acts to resolve inflammation.
Insights
Pentraxin-3 (PTX3) regulates macrophage activity by reducing inflammatory cytokines like IL-1β and TNF-α. This suggests PTX3 plays a key role in resolving inflammation and offers therapeutic potential.
Area of Science:
- Immunology
- Molecular Biology
- Biochemistry
Background:
- Pentraxin-3 (PTX3) is implicated in cardiovascular diseases and vascular inflammation.
- The precise functions of PTX3 in inflammatory processes, particularly within macrophages, remain incompletely understood.
Purpose of the Study:
- To elucidate the functional role of Pentraxin-3 (PTX3) in modulating macrophage inflammatory responses.
- To investigate PTX3's impact on cytokine production, signaling pathways, and phagocytic activity in macrophages.
Main Methods:
- Recombinant PTX3 was applied to THP-1 macrophages and primary human macrophages.
- Cytokine and chemokine levels (IL-1β, TNF-α, MCP-1) were quantified.
- PTX3-silenced apoptotic macrophages were utilized to assess phagocytosis and surface marker expression (HLA-DR, CD86).
Main Results:
- PTX3 significantly reduced macrophage-derived IL-1β, TNF-α, and MCP-1 levels, while inducing TGF-β activation.
- PTX3 inhibited NF-κB activation and promoted Akt phosphorylation.
- Silencing PTX3 in apoptotic macrophages enhanced binding and increased HLA-DR and CD86 expression, alongside IL-1β production.
Conclusions:
- Pentraxin-3 (PTX3) functions as a novel regulator of macrophage activity.
- PTX3's anti-inflammatory effects suggest a crucial role in inflammation resolution.
More Related Videos
07:55A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces
Published on: January 7, 2020
08:08In Vitro Stimulation and Visualization of Extracellular Trap Release in Differentiated Human Monocyte-derived Macrophages
Published on: November 1, 2019
Related Concept Videos
01:38Inflammation
01:28Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...