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Updated: Jun 16, 2026
Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Stretch regulated surface roughness controls macrophage inflammatory polarization through adhesion-chromatin
Gang Yang1, Yi Han2, Tao Tang3
1Department of General Surgery, Affiliated Hospital of North Sichuan Medical College, National Clinical Key Specialty (General Surgery), Sichuan Branch of National Clinical Research Center for Digestive Diseases, Sichuan Clinical Research Center for Digestive Diseases, Nanchong, China.
Surface roughness mechanically controls macrophage inflammation. This study found that smoother biomaterial surfaces promote pro-inflammatory responses by altering cell adhesion and chromatin organization, influencing immune cell behavior at material interfaces.
Area of Science:
- Biomaterials Science
- Cellular Biology
- Immunology
Background:
- Macrophages are key immune cells at biomaterial interfaces.
- Distinguishing surface roughness effects from substrate stiffness is challenging.
- Understanding roughness's role in macrophage inflammatory responses is crucial.
Purpose of the Study:
- Isolate and clarify the role of surface roughness in macrophage inflammatory programming.
- Investigate how surface roughness influences macrophage-material interactions.
- Determine if roughness is a tunable regulator of macrophage phenotype.
Main Methods:
- Developed a magnetic stretching device to tune polydimethylsiloxane (PDMS) membrane roughness.
- Utilized atomic force microscopy to characterize surface topography and stiffness.
- Cultured RAW264.7 macrophages to assess morphology, signaling, gene expression, and function; validated on NaOH-treated glass.
Main Results:
- Reduced PDMS surface roughness enhanced macrophage spreading and focal adhesion kinase signaling.
- Smoother surfaces led to increased chromatin density and decreased accessibility.
- Pro-inflammatory phenotypes (TNF, IL-1 expression, TNF-α secretion) and phagocytic activity were elevated on smoother surfaces.
- Roughness modulation consistently affected macrophage behavior across different material platforms.
Conclusions:
- Surface roughness is a mechanically tunable regulator of macrophage inflammatory polarization.
- Roughness-dependent cell-material adhesion may influence chromatin organization and accessibility.
- This suggests an adhesion-associated chromatin mechanism for macrophage inflammatory programming at biomaterial interfaces.
