Biomaterial adherent macrophage apoptosis is increased by hydrophilic and anionic substrates in vivo
Open accessAbstract
An in vivo rat cage implant system was used to identify potential surface chemistries that prevent failure of implanted biomedical devices and prostheses by limiting monocyte adhesion and macrophage fusion into foreign-body giant cells while inducing adherent-macrophage apoptosis. Hydrophobic, hydrophilic, anionic, and cationic surfaces were used for implantation. Analysis of the exudate surrounding the materials revealed no differences between surfaces in the types or levels of cells present. Conversely, the proportion of adherent cells undergoing apoptosis was increased significantly on anionic and hydrophilic surfaces (46 ± 3.7 and 57 ± 5.0%, respectively) when compared with the polyethylene terephthalate base surface. Additionally, hydrophilic and anionic substrates provided decreased rates of monocyte/macrophage adhesion and fusion. These studies demonstrate that biomaterial-adherent cells undergo material-dependent apoptosis in vivo , rendering potentially harmful macrophages nonfunctional while the surrounding environment of the implant remains unaffected.
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Biomaterial surface chemistry influences apoptosis of adherent macrophages both in vitro and in vivo.
“Biomaterial surface chemistry influences apoptosis of adherent macrophages both in vitro and in vivo.[12, 53–55]”
From Foreign body reaction to biomaterials (2008) · cites this paper as [54]
The Results (page not provided) show that surface chemistry affected adherent-macrophage apoptosis in vivo. The paper also reports in its introductory text (page not provided) an earlier in vitro finding for biomaterial-adherent cells, but does not specify there that those cells were macrophages. Thus, the in vitro macrophage-specific part is not established by our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredAdherent inflammatory cell apoptosis is an important mechanism for the persistence of cardiovascular device infection where apoptosis is induced by shear stress in cardiovascular devices.
“Adherent inflammatory cell apoptosis has been described as an important mechanism for the persistence of cardiovascular device infection where apoptosis is induced by shear stress in cardiovascular devices.[54]”
From Foreign body reaction to biomaterials (2008) · cites this paper as [54]
The Abstract (page unavailable) reports that fluid shear stress causes apoptosis of biomaterial-adherent neutrophils and says this may increase cardiovascular prostheses’ susceptibility to bacterial infection. It does not establish apoptosis as an important mechanism for the persistence of an existing device infection; that is stronger and more specific than the paper’s tentative statement. (LLM, conf=0.87)
Experimental — accuracy not yet measuredHydrophilic, anionic surfaces promote the highest levels of apoptosis of biomaterial adherent FBGC.
“In a previous study by Brodbeck et al. [50], it was reported that hydrophilic, anionic surfaces promoted the highest levels of apoptosis of biomaterial adherent FBGC.”
From Biomaterial based modulation of macrophage polarization: a review and suggested design principles (2015) · cites this paper as [50]
Inducing apoptosis in adhered FBGC would reduce the negative effects of adhered cells and improve tissue remodeling.
“Since FBGC are detrimental to the biomaterial due to their ability to increase oxidative damage and recruit other inflammatory cells, the authors proposed that inducing apoptosis in the adhered FBGC would reduce the negative effects of adhered cells and improve tissue remodeling [50,51].”
From Biomaterial based modulation of macrophage polarization: a review and suggested design principles (2015) · cites this paper as [50]
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- Authors
- Brodbeck, W. G., Patel, J., Voskerician, G., Christenson, E., Shive, M. S., Nakayama, Y., Matsuda, T., Ziats, N. P., & Anderson, J. M.
- Affiliations
- Kyushu University (JP)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2002-07-16
- Volume
- 99
- Issue
- 16
- Pages
- 10287-10292
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC124906
- OpenAlex
- W2016639612
- Cited by
- 245
- References
- 21
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 10 · 2023: 4 · 2022: 5 · 2021: 12 · 2020: 13 · 2019: 15 · 2018: 8 · 2017: 11 · 2016: 11 · 2015: 9 · 2014: 7 · 2013: 7 · 2012: 16
- FWCI
- 5.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (HL-33849)
- National Heart, Lung, and Blood Institute (HL55714, R01HL055714, HL 33849)
- National Institute of General Medical Sciences (GM-20380, F32GM020380)
- Topics
- Physical Sciences › Materials Science › Surfaces, Coatings and Films › Polymer Surface Interaction Studies
- Health Sciences › Medicine › Surgery › Orthopaedic implants and arthroplasty
- Physical Sciences › Engineering › Biomedical Engineering › Bone Tissue Engineering Materials
- Keywords
- macrophage apoptosis, foreign body giant cells, hydrophilic surfaces, anionic surfaces, hydrophobic surfaces, cationic surfaces, monocyte adhesion, macrophage fusion, implant biocompatibility, cage implantation, polyethylene terephthalate, exudate
- MeSH terms
- Animals, Anions, Cell Adhesion, Female, Macrophages, Rats, Sprague-Dawley, Apoptosis, Coated Materials, Biocompatible, Rats, Hydrophobic and Hydrophilic Interactions
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