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Updated: May 3, 2026
Fragmenting Bulk Hydrogels and Processing into Granular Hydrogels for Biomedical Applications
Published on: May 17, 2022
Poly(ethylene glycol)-containing hydrogels promote the release of primary granules from human blood-derived
Hannah Caitlin Cohen1, Tyler Jacob Lieberthal, W John Kao
1Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, 777 Highland Avenue, Madison, Wisconsin, 53705.
Abstract:
Polymorphonuclear leukocytes (PMNs) are recruited to sites of injury and biomaterial implants. Once activated, PMNs can exocytose their granule subsets to recruit monocytes (MCs) and mediate MC/macrophage activation. We investigated the release of myeloperoxidase (MPO), a primary granule marker, and matrix metalloproteinase-9 (MMP-9), a tertiary granule marker, from human blood-derived PMNs cultured on poly(ethylene glycol) (PEG) hydrogels, polydimethylsiloxane (PDMS), tissue culture polystyrene (TCPS) and gelatin-PEG (GP) hydrogels, with and without the presence of the bacterial peptide formyl-Met-Leu-Phe. Supernatants from PMN cultures on PEG-containing hydrogels (i.e., PEG and GP hydrogels) had higher concentrations of MPO than those from PMN cultures on PDMS or TCPS at 2 h. PMNs on all biomaterials released comparable levels of MMP-9 at 2 h, indicating that PMNs cultured on PEG-containing hydrogels have different mechanisms of release for primary and tertiary granules. Src family kinases were involved in the release of MPO from PMNs cultured on PEG hydrogels, TCPS and GP hydrogels and in the release of MMP-9 from PMNs cultured on all four biomaterials. The increased release of primary granules from PMNs on PEG-containing hydrogels did not significantly increase MC chemotaxis, indicating that additional co-effectors in the dynamic inflammatory milieu in vivo modulate PMN-mediated MC recruitment.
Insights
Poly(ethylene glycol) hydrogels increase the release of primary granules from polymorphonuclear leukocytes (PMNs), but do not significantly enhance monocyte (MC) recruitment, suggesting in vivo factors modulate this response.
Area of Science:
- Biomaterials Science
- Immunology
- Cell Biology
Background:
- Polymorphonuclear leukocytes (PMNs) are crucial immune cells recruited to injury sites and biomaterials.
- Activated PMNs release granule contents to recruit and activate monocytes (MCs), influencing inflammation.
- Understanding PMN-biomaterial interactions is key to controlling inflammatory responses.
Purpose of the Study:
- To investigate the differential release of PMN granule markers (MPO and MMP-9) on various biomaterials.
- To explore the role of Src family kinases in PMN degranulation on different material surfaces.
- To assess the impact of PMN activation on PEG-hydrogel surfaces on subsequent monocyte chemotaxis.
Main Methods:
- Human blood-derived PMNs were cultured on poly(ethylene glycol) (PEG) hydrogels, gelatin-PEG (GP) hydrogels, polydimethylsiloxane (PDMS), and tissue culture polystyrene (TCPS).
- Myeloperoxidase (MPO) and matrix metalloproteinase-9 (MMP-9) release were quantified in culture supernatants.
- The effect of the bacterial peptide formyl-Met-Leu-Phe on PMN activation was evaluated.
- Involvement of Src family kinases was assessed.
- Monocyte chemotaxis assays were performed using PMN supernatants.
Main Results:
- PMNs cultured on PEG-containing hydrogels (PEG and GP) showed significantly higher myeloperoxidase (MPO) release compared to PDMS and TCPS at 2 hours.
- Matrix metalloproteinase-9 (MMP-9) release was comparable across all tested biomaterials at 2 hours.
- Src family kinases were implicated in MPO release on PEG hydrogels, TCPS, and GP hydrogels, and in MMP-9 release on all materials.
- Enhanced MPO release from PMNs on PEG-hydrogels did not lead to a significant increase in monocyte chemotaxis.
Conclusions:
- PMN degranulation mechanisms differ for primary (MPO) and tertiary (MMP-9) granules on PEG-containing hydrogels.
- Src family kinases play a role in PMN degranulation across various biomaterial surfaces.
- While PEG-hydrogels can enhance PMN primary granule release, this does not directly translate to increased monocyte recruitment, indicating complex in vivo regulation.
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