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Updated: Mar 15, 2026

A Multi-Cue Bioreactor to Evaluate the Inflammatory and Regenerative Capacity of Biomaterials under Flow and Stretch
Published on: December 10, 2020
Solubilized extracellular matrix bioscaffolds derived from diverse source tissues differentially influence macrophage
Jenna L Dziki1,2, Derek S Wang1, Catalina Pineda1,2
1McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.
Extracellular matrix (ECM) biomaterials modulate macrophage responses. Certain ECM sources, like small intestinal submucosa (SIS), promote constructive tissue remodeling by inducing an anti-inflammatory M2 macrophage phenotype.
Area of Science:
- Biomaterials Science
- Immunology
- Tissue Engineering
Background:
- Host response to biomaterials is crucial for tissue repair.
- Macrophages are key responders and predictors of tissue remodeling.
- Mammalian extracellular matrix (ECM) biomaterials promote constructive remodeling by modulating macrophage responses.
Purpose of the Study:
- To investigate the differential effects of ECM bioscaffolds from eight different source tissues on macrophage behavior.
- To analyze changes in macrophage surface marker expression, protein content, phagocytosis, metabolism, and antimicrobial activity.
Main Methods:
- Decellularization of eight distinct tissue sources to create ECM bioscaffolds.
- Exposure of macrophages to these ECM bioscaffolds.
- Analysis of macrophage phenotype (M1/M2 markers), protein content, phagocytic capability, metabolism, and antimicrobial activity.
Main Results:
- ECM bioscaffolds from small intestinal submucosa (SIS), urinary bladder matrix (UBM), brain ECM (bECM), esophageal ECM (eECM), and colonic ECM (coECM) induced a pro-remodeling, anti-inflammatory M2-like macrophage phenotype.
- Dermal ECM induced a pro-inflammatory M1-like phenotype.
- Liver ECM (LECM) and skeletal muscle ECM (mECM) did not significantly alter M1/M2 marker expression.
- All ECM treatments increased macrophage antimicrobial activity.
- Macrophage metabolism was decreased by UBM, bECM, mECM, coECM, and dermal ECM.
Conclusions:
- Different ECM sources elicit distinct macrophage responses, influencing tissue remodeling outcomes.
- SIS, UBM, bECM, eECM, and coECM show potential for promoting constructive, anti-inflammatory tissue repair.
- Understanding these source-specific macrophage modulations is vital for selecting appropriate ECM biomaterials for site-specific tissue regeneration.
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