ArticleJournal of biomedical materials research. Part A2012
Effect of macrophage classical (M1) activation on implant-adherent macrophage interactions with Staphylococcus epidermidis: A murine in vitro model system.
Article in Journal of biomedical materials research. Part A, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Fine-Tuned Functionalizable Terpolymer Brush Nanocoating Resists Protein Adsorption and Bacterial Adhesion while Promoting Macrophage Activity and Osteoblast Proliferation.ACS applied materials & interfaces · 2025Article
- Modelling of macrophage responses to biomaterialsFrontiers in immunology · 2024Review
- Mangiferin inhibits macrophage classical activation via downregulating interferon regulatory factor 5 expression.Molecular medicine reports · 2016Article
- HCV core protein binds to gC1qR to induce A20 expression and inhibit cytokine production through MAPKs and NF-κB signaling pathways.Oncotarget · 2016Article
- Ventricular shunt infections: immunopathogenesis and clinical management.Journal of neuroimmunology · 2014Review
- Increase in hypotonic stress-induced endocytic activity in macrophages via ClC-3.Molecules and cells · 2014Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
A model in vitro system was developed for eliciting classical (M1) activation of surface-adherent murine macrophages, which was then used to study the interaction of the M1 macrophages with Staphylococcus epidermidis. Glass substrata were first covalently grafted with a mixture of methoxy- and biotin-terminated silanated polyethylene glycol. Interferon (IFN)-γ and/or lipopolysaccharide (LPS), ligands known to induce the highly microbicidal M1 activation state in macrophages, were biotinylated and immobilized by way of a streptavidin intermediate to the biotin-PEG base substratum. Assessment of mouse bone marrow-derived macrophage (BMDM) interleukin (IL)-12(p40) and nitric oxide response to the fabricated surfaces confirmed that the model system achieved activation of adherent macrophage: IFN-γ-presenting surfaces primed cells for M1 activation, LPS-presenting surfaces elicited innate activation, and surface presenting a combination of IFN-γ and LPS induced M1 activation. The phagocytic and microbicidal capacity of activated, surface-adherent BMDM was evaluated using S. epidermidis, a bacterial species prevalent in implant-associated infections. Results indicate that M1 activation of implant-adherent macrophages trends towards diminishing their phagocytic capacity, but enhances their microbicidal capacity for S. epidermidis.
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