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Updated: Jun 27, 2026
Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
CCL17-neutralizing and esterase-responsive core-shell microgels for endogenous Tregs recruitment and functional
Liang Song1, Yongyuan Kang1, Pai Peng1
1Zhejiang Key Laboratory of Advanced Organic Materials and Technologies, MOE Key Laboratory of Macromolecular Synthesis and Functionalization, International Research Center for X Polymers, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, 310058, China.
Myocardial infarction (MI) disrupts immune homeostasis by impairing the recruitment and suppressive function of regulatory T cells (Tregs), which are hard to restore to date. In this study, a dual-functional platform based on core-shell microgels (Ab/HAPA C-S MGs) was developed to enhance Tregs homing and function within the post-infarct environment. The surface-modified C-C motif chemokine ligand 17 (CCL17) antibody neutralized excess CCL17, thereby enabling targeted Tregs recruitment. Propionic acid (PA) was released via hydrolytic cleavage of an encapsulated prodrug precursor (HAPA) within the core to promote Tregs immunosuppressive activity through fatty acid oxidation. The platform ensured localized retention and release of PA, addressing the pharmacokinetic limitations characteristic of short-chain fatty acid (SCFAs). The Ab/HAPA@C-S MGs enhanced Tregs recruitment by 4.2-fold through CCL17 neutralization, while enzymatically released PA boosted Tregs immunosuppression with 1.8-fold higher Foxp3 expression in vitro. In MI models, treatment with Ab/HAPA@C-S MGs promoted a 2.4-fold increase in Tregs infiltration while reducing Th17 cells in infarcted region, ultimately improving cardiac functions and attenuating myocardial fibrosis. These findings show potential of the SCFA-based C-S MGs system on regulating the immunomodulation and cardiac tissue repair.
Myocardial infarction (MI) disrupts immune homeostasis by impairing the recruitment and suppressive function of regulatory T cells (Tregs), which are hard to restore to date. In this study, a dual-functional platform based on core-shell microgels (Ab/HAPA C-S MGs) was developed to enhance Tregs homing and function within the post-infarct environment. The surface-modified C-C motif chemokine ligand 17 (CCL17) antibody neutralized excess CCL17, thereby enabling targeted Tregs recruitment. Propionic acid (PA) was released via hydrolytic cleavage of an encapsulated prodrug precursor (HAPA) within the core to promote Tregs immunosuppressive activity through fatty acid oxidation. The platform ensured localized retention and release of PA, addressing the pharmacokinetic limitations characteristic of short-chain fatty acid (SCFAs). The Ab/HAPA@C-S MGs enhanced Tregs recruitment by 4.2-fold through CCL17 neutralization, while enzymatically released PA boosted Tregs immunosuppression with 1.8-fold higher Foxp3 expression in vitro. In MI models, treatment with Ab/HAPA@C-S MGs promoted a 2.4-fold increase in Tregs infiltration while reducing Th17 cells in infarcted region, ultimately improving cardiac functions and attenuating myocardial fibrosis. These findings show potential of the SCFA-based C-S MGs system on regulating the immunomodulation and cardiac tissue repair.
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