Effect of macrophage classical (M1) activation on implant-adherent macrophage interactions with Staphylococcus epidermidis: A murine in vitro model system.
Effect of macrophage classical (M1) activation on implant-adherent macrophage interactions with Staphylococcus epidermidis: A murine in vitro model system.
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DOI:
10.1002/jbm.a.34087
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发表时间:
2012-08
影响因子:
4.9
通讯作者:
Bryers, James D.
中科院分区:
文献类型:
--
作者:
Park, Kyung R.;Bryers, James D.
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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影响因子:
4.9
作者:
Schmidt, David Richard;Kao, Weiyuan John
通讯作者:
Kao, Weiyuan John
影响因子:
2.9
作者:
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DOI:
10.1016/j.cimid.2009.07.001
发表时间:
2010-09
期刊:
Comparative immunology, microbiology and infectious diseases
影响因子:
--
作者:
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通讯作者:
Boons GJ
影响因子:
4.4
作者:
Stout, RD;Jiang, CC;Suttles, J
通讯作者:
Suttles, J