The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
James M. Anderson - One of the best experts on this subject based on the ideXlab platform.
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In vivo quantitative and qualitative assessment of foreign Body Giant Cell formation on biomaterials in mice deficient in natural killer lymphocyte subsets, mast Cells, or the interleukin‐4 receptorα and in severe combined immunodeficient mice
Journal of Biomedical Materials Research Part A, 2014Co-Authors: Junghoon Yang, Amy K. Mcnally, Brian Jao, James M. AndersonAbstract:In previous studies that explored the influence of cytokines on foreign Body Giant Cell (FBGC) formation, we focused on interleukin (IL)−4 and IL-13, each of which was discovered to induce macrophage fusion leading to FBGC formation in vitro. Two correlative in vivo studies also confirmed that IL-4 plays a role in FBGC formation on implanted biomaterials, but that T lymphocytes are not the source of IL-4 or other cytokines that support this process. The present study focused on identification of the Cellular source of macrophage fusion-inducing cytokines, including natural killer (NK) or NKT lymphocytes and mast Cells using mouse models genetically deficient in each of these Cell types, as well as IL-4 receptor alpha(IL-4Rα)-deficient and severe combined immunodeficient (SCID) mice. Polyetherurethane (PEU) and polyethylene terephthalate (PET) polymers were subcutaneously implanted and retrieved after 14, 21, or 28 days. FBGC formation was evaluated using quantitative and qualitative data from retrieved polymer surfaces. Both types of data indicate that, compared to normal control mice, neither NK or NKT lymphocytes nor mast Cells are required for FBGC formation. Furthermore, FBGC formation on biomaterials can proceed in IL-4Rα-deficient and in SCID mice. Similar conclusions were made regarding FBGC formation on both PEU and PET biomaterials. These data suggest that other sources of IL-4/IL-13 and/or additional macrophage fusion-inducing cytokines can mediate FBGC formation on implanted biomaterials, or that, in the absence of normal primary pathways, FBGC formation is nevertheless supported by redundant innate mechanisms. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 2017–2023, 2014.
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In Vitro and In Vivo Monocyte, Macrophage, Foreign Body Giant Cell, and Lymphocyte Interactions with Biomaterials
Biological Interactions on Materials Surfaces, 2009Co-Authors: James M. AndersonAbstract:This chapter focuses on recent developments in our understanding of in vitro and in vivo monocyte, macrophage, foreign Body Giant Cell (FBGC), and lymphocyte interactions with biomaterials in the context of inflammatory and wound-healing responses following implantation of biomaterials, medical devices, and prostheses. Quantitative studies identify the significance of biomaterial surface chemistry in modulating inflammatory Cell behaviors such as adhesion, apoptosis, anoikis, fusion, and cytokine secretion. Utilizing genomic and proteomic techniques, Cell-Cell (juxtacrine) and cytokine-mediated (paracrine) responses between Cells have been identified. Consequences of the persistence of the foreign Body reaction, i.e., macrophages and FBGCs, at the tissue-material interface are presented. Given the current and future use of new approaches, such as nanotechnology and tissue engineering, the continuing development of a mechanistic understanding of inflammatory Cell interactions with biomaterials is necessary.
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Paracrine and juxtacrine lymphocyte enhancement of adherent macrophage and foreign Body Giant Cell activation.
Journal of Biomedical Materials Research Part A, 2009Co-Authors: David T. Chang, Erica Colton, James M. AndersonAbstract:Lymphocytes have been shown to be involved in modulating monocyte and macrophage behavior in the foreign Body reaction. Lymphocyte effects on biomaterial-adherent macrophage and foreign Body Giant Cell (FBGC) behavior were further investigated by culturing monocytes alone or together with lymphocytes, either in direct co-cultures or indirectly in transwells, on a series of polyethylene terephthalate (PET)-based photograft co-polymerized material surfaces displaying distinct hydrophobic, hydrophilic/neutral, hydrophilic/anionic, and hydrophilic/cationic chemistries. After periods of 3, 7, and 10 days, cytokine production was quantified by ELISA and normalized to adherent macrophage/FBGC density to yield a measure of adherent macrophage/FBGC activation. Interactions with lymphocytes enhanced adherent macrophage and FBGC production of pro-inflammatory IL-1β, TNF-α, IL-6, IL-8, and MIP-1β on the hydrophobic and hydrophilic/cationic surfaces but had no effect on anti-inflammatory IL-10 production indicating lymphocytes promote a pro-inflammatory response to biomaterials. Lymphocytes also did not significantly influence MMP-9, TIMP-1, and TIMP-2 production. Interactions through indirect (paracrine) signaling showed a significant effect in enhancing adherent macrophage/FBGC activation at early time points while interactions via direct (juxtacrine) mechanisms dominated at later time points. Biomaterial surface chemistries differentially affected the observed responses as hydrophilic/neutral and hydrophilic/anionic surfaces evoked the highest levels of activation relative to the other surfaces but did not facilitate lymphocyte enhancement of adherent macrophage/FBGC activation.
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vitronectin is a critical protein adhesion substrate for il 4 induced foreign Body Giant Cell formation
Journal of Biomedical Materials Research Part A, 2008Co-Authors: Amy K. Mcnally, Jacqueline A. Jones, Sarah R. Macewan, Erica Colton, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced foreign Body Giant Cell (FBGC) formation was utilized to define the adhesion protein substrate(s) that promotes this aspect of the foreign Body reaction on biomedical polymers. Human monocytes were cultured on Cell culture polystyrene surfaces that had been pre-adsorbed with a synthetic arginine-glycine-aspartate peptide previously found to support optimal FBGC formation, or with various concentrations of potential physiological protein substrates, i.e. complement C3bi, collagen types I or IV, fibrinogen, plasma fibronectin, fibroblast fibronectin, laminin, thrombospondin, vitronectin, or von Willebrand factor. Cultures were evaluated on days 0 (1.5 h), 3, and 7 by May–Grunwald/Giemsa staining. Initial monocyte adhesion occurred on all adsorbed proteins. However, by day 7 of culture, only vitronectin was striking in its ability to support significant macrophage adhesion, development, and fusion leading to FBGC formation. Vitronectin supported high degrees of FBGC formation at an absorption concentration between 5 and 25 μg/mL. These findings suggest that adsorbed vitronectin is critical in the collective events that support and promote FBGC formation on biomedical polymers, and that the propensity for vitronectin adsorption may underlie the material surface chemistry dependency of FBGC formation. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2008
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Vitronectin is a critical protein adhesion substrate for IL-4-induced foreign Body Giant Cell formation.
Journal of Biomedical Materials Research Part A, 2008Co-Authors: Amy K. Mcnally, Jacqueline A. Jones, Sarah R. Macewan, Erica Colton, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced foreign Body Giant Cell (FBGC) formation was utilized to define the adhesion protein substrate(s) that promotes this aspect of the foreign Body reaction on biomedical polymers. Human monocytes were cultured on Cell culture polystyrene surfaces that had been pre-adsorbed with a synthetic arginine-glycine-aspartate peptide previously found to support optimal FBGC formation, or with various concentrations of potential physiological protein substrates, i.e. complement C3bi, collagen types I or IV, fibrinogen, plasma fibronectin, fibroblast fibronectin, laminin, thrombospondin, vitronectin, or von Willebrand factor. Cultures were evaluated on days 0 (1.5 h), 3, and 7 by May-Grunwald/Giemsa staining. Initial monocyte adhesion occurred on all adsorbed proteins. However, by day 7 of culture, only vitronectin was striking in its ability to support significant macrophage adhesion, development, and fusion leading to FBGC formation. Vitronectin supported high degrees of FBGC formation at an absorption concentration between 5 and 25 microg/mL. These findings suggest that adsorbed vitronectin is critical in the collective events that support and promote FBGC formation on biomedical polymers, and that the propensity for vitronectin adsorption may underlie the material surface chemistry dependency of FBGC formation.
Amy K. Mcnally - One of the best experts on this subject based on the ideXlab platform.
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In vivo quantitative and qualitative assessment of foreign Body Giant Cell formation on biomaterials in mice deficient in natural killer lymphocyte subsets, mast Cells, or the interleukin‐4 receptorα and in severe combined immunodeficient mice
Journal of Biomedical Materials Research Part A, 2014Co-Authors: Junghoon Yang, Amy K. Mcnally, Brian Jao, James M. AndersonAbstract:In previous studies that explored the influence of cytokines on foreign Body Giant Cell (FBGC) formation, we focused on interleukin (IL)−4 and IL-13, each of which was discovered to induce macrophage fusion leading to FBGC formation in vitro. Two correlative in vivo studies also confirmed that IL-4 plays a role in FBGC formation on implanted biomaterials, but that T lymphocytes are not the source of IL-4 or other cytokines that support this process. The present study focused on identification of the Cellular source of macrophage fusion-inducing cytokines, including natural killer (NK) or NKT lymphocytes and mast Cells using mouse models genetically deficient in each of these Cell types, as well as IL-4 receptor alpha(IL-4Rα)-deficient and severe combined immunodeficient (SCID) mice. Polyetherurethane (PEU) and polyethylene terephthalate (PET) polymers were subcutaneously implanted and retrieved after 14, 21, or 28 days. FBGC formation was evaluated using quantitative and qualitative data from retrieved polymer surfaces. Both types of data indicate that, compared to normal control mice, neither NK or NKT lymphocytes nor mast Cells are required for FBGC formation. Furthermore, FBGC formation on biomaterials can proceed in IL-4Rα-deficient and in SCID mice. Similar conclusions were made regarding FBGC formation on both PEU and PET biomaterials. These data suggest that other sources of IL-4/IL-13 and/or additional macrophage fusion-inducing cytokines can mediate FBGC formation on implanted biomaterials, or that, in the absence of normal primary pathways, FBGC formation is nevertheless supported by redundant innate mechanisms. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 2017–2023, 2014.
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Vitronectin is a critical protein adhesion substrate for IL-4-induced foreign Body Giant Cell formation.
Journal of Biomedical Materials Research Part A, 2008Co-Authors: Amy K. Mcnally, Jacqueline A. Jones, Sarah R. Macewan, Erica Colton, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced foreign Body Giant Cell (FBGC) formation was utilized to define the adhesion protein substrate(s) that promotes this aspect of the foreign Body reaction on biomedical polymers. Human monocytes were cultured on Cell culture polystyrene surfaces that had been pre-adsorbed with a synthetic arginine-glycine-aspartate peptide previously found to support optimal FBGC formation, or with various concentrations of potential physiological protein substrates, i.e. complement C3bi, collagen types I or IV, fibrinogen, plasma fibronectin, fibroblast fibronectin, laminin, thrombospondin, vitronectin, or von Willebrand factor. Cultures were evaluated on days 0 (1.5 h), 3, and 7 by May-Grunwald/Giemsa staining. Initial monocyte adhesion occurred on all adsorbed proteins. However, by day 7 of culture, only vitronectin was striking in its ability to support significant macrophage adhesion, development, and fusion leading to FBGC formation. Vitronectin supported high degrees of FBGC formation at an absorption concentration between 5 and 25 microg/mL. These findings suggest that adsorbed vitronectin is critical in the collective events that support and promote FBGC formation on biomedical polymers, and that the propensity for vitronectin adsorption may underlie the material surface chemistry dependency of FBGC formation.
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vitronectin is a critical protein adhesion substrate for il 4 induced foreign Body Giant Cell formation
Journal of Biomedical Materials Research Part A, 2008Co-Authors: Amy K. Mcnally, Jacqueline A. Jones, Sarah R. Macewan, Erica Colton, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced foreign Body Giant Cell (FBGC) formation was utilized to define the adhesion protein substrate(s) that promotes this aspect of the foreign Body reaction on biomedical polymers. Human monocytes were cultured on Cell culture polystyrene surfaces that had been pre-adsorbed with a synthetic arginine-glycine-aspartate peptide previously found to support optimal FBGC formation, or with various concentrations of potential physiological protein substrates, i.e. complement C3bi, collagen types I or IV, fibrinogen, plasma fibronectin, fibroblast fibronectin, laminin, thrombospondin, vitronectin, or von Willebrand factor. Cultures were evaluated on days 0 (1.5 h), 3, and 7 by May–Grunwald/Giemsa staining. Initial monocyte adhesion occurred on all adsorbed proteins. However, by day 7 of culture, only vitronectin was striking in its ability to support significant macrophage adhesion, development, and fusion leading to FBGC formation. Vitronectin supported high degrees of FBGC formation at an absorption concentration between 5 and 25 μg/mL. These findings suggest that adsorbed vitronectin is critical in the collective events that support and promote FBGC formation on biomedical polymers, and that the propensity for vitronectin adsorption may underlie the material surface chemistry dependency of FBGC formation. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2008
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α subunit partners to β1 and β2 integrins during IL-4-induced foreign Body Giant Cell formation
Journal of Biomedical Materials Research Part A, 2007Co-Authors: Amy K. Mcnally, Sarah R. Macewan, James M. AndersonAbstract:As beta1 and beta2 integrins were previously found to mediate adhesion during IL-4-induced foreign Body Giant Cell (FBGC) formation, we pursued the identities of the alpha integrin partners of these adhesion receptors using our in vitro system of human monocyte-derived macrophage fusion. Immunoprecipitation with beta1 and immunoblotting reveal the presence of alpha5 and alphaV, as well as alpha2 and alpha3. alphaM and alphaX immunoprecipitate with beta2 but not with beta1. Immunocytochemistry coupled with confocal microscopy indicates that alpha5 and alphaX are poorly expressed on day 0. However, following the induction of fusion by IL-4 on day 3, they are each readily detectable in fusing macrophages/FBGC on day 7. In contrast, alphaM and alphaV are present throughout the culture period, with very strong alphaM expression on day 7. We also demonstrate expression and colocalization of alpha3, alpha5, or alphaV with beta1 on fusing macrophages/FBGC at this time point as well as strong colocalization of alphaM and alphaX with beta2 in FBGC and at fusion interfaces. Therefore, IL-4-induced FBGC are characterized by the expression of alphaMbeta2, alphaXbeta2, alpha5beta1, alphaVbeta1, alpha2beta1, and alpha3beta1, which indicates potential interactions with fragments of complement C3, fibrin(ogen), fibronectin, Factor X, and vitronectin, and possibly with certain collagens, laminin, and thrombospondin at sites of biomaterial implantation.
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β1 and β2 Integrins Mediate Adhesion during Macrophage Fusion and Multinucleated Foreign Body Giant Cell Formation
American Journal of Pathology, 2002Co-Authors: Amy K. Mcnally, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced human monocyte-derived macrophage fusion was used to investigate the Cell/substrate adhesive mechanisms that support multinucleated foreign Body Giant Cell (FBGC) formation. Monocytes were cultured for 3 days and IL-4 was added to induce macrophage fusion and FBGC formation by day 7. Functionally defined anti-integrin antibodies demonstrated that initial monocyte adhesion is mediated by β2 integrins, whereas during the induction of macrophage fusion by IL-4, an additional dependence on β1 integrins is acquired. The combination of anti-β1 plus anti-β2 was most effective, reducing macrophage/FBGC adhesion to 10% of controls. Consistent with integrin-mediated signaling, the tyrosine kinase inhibitor genistein and the phosphatidylinositol-3-kinase inhibitors wortmannin and LY294002 also attenuated macrophage/FBGC adhesion. Confocal microscopic analysis revealed that β2 integrins are present on monocytes after initial adhesion and are strongly expressed on fusing macrophages, particularly in peripheral Cell areas, and on FBGCs. In contrast, β1 integrins are not detected on monocytes but begin to appear during macrophage development and are strongly expressed on fusing macrophages and FBGCs. For the first time, these results demonstrate the IL-4-induced acquisition of cooperation between β1 and β2 integrins in the Cell/substrate adhesive interactions that are required for multinucleated FBGC formation.
Weiyuan John Kao - One of the best experts on this subject based on the ideXlab platform.
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Theoretical analysis of in vivo macrophage adhesion and foreign Body Giant Cell formation on polydimethylsiloxane, low density polyethylene, and polyetherurethanes
Journal of Biomedical Materials Research, 2004Co-Authors: Weiyuan John Kao, Anne Hiltner, Qing H. Zhao, James M. AndersonAbstract:Quantitative description of foreign Body Giant Cell (FBGC) formation on implanted polymer surfaces as a function of time can conceivably correlate Cell adhesion with polymer properties and possibly predict the behavior of the polymer in vivo. In the present study, the formation of FBGCs on various biomedical polymers was quantified by two parameters: the density of adherent macrophages present initially that participate in FBGC formation (d0) and the rate constant for Cell fusion (k); both kinetic parameters were used to calculate the time-dependent FBGC density (dfc). The materials used were: three Pellethane poly(etherurethanes) (PEUs) varying in weight percent of hard segment, one poly(etherurethane urea) (PEUU), and NHLBI-DTB primary reference materials: low density polyethylene (LDPE), silica-free polydimethylsiloxane (PDMS). The results indicated that up to 5 weeks of implantation, FBGCs were formed from the fusion of one population of adherent macrophages present by 3 days post-implantation. Furthermore, only a small fraction (< 8%) of this initial adherent macrophage population participated in FBGC formation. Based on the results of previous studies and the current study, it was concluded that increase in PEU hard segment weight percent, surface hardness and hydrophobicity increased total protein adsorption and effectively increased d0 and dfc. No further correlations between the material properties of all polymers and the Cell kinetics can be made at this time. However, this study demonstrated that macrophage adhesion and FBGC formation can be quantified with the Cell fusion model, and are modulated by various polymer properties.
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Role for interleukin‐4 in foreign‐Body Giant Cell formation on a poly(etherurethane urea) in vivo
Journal of Biomedical Materials Research, 1995Co-Authors: Weiyuan John Kao, Amy K. Mcnally, Anne Hiltner, James M. AndersonAbstract:Interleukin-4 (IL-4) was previously shown to induce extensive macrophage fusion to form foreign-Body Giant Cells (FBGCs) in vitro. In the present study, our goal was to extend these findings to an in vivo test environment on biomaterials. The subcutaneous cage-implant system was modified for mice to elucidate IL-4 participation in mediating FBGC formation in vivo. Exudate leukocyte concentrations from cages containing poly(etherurethane urea) (PEUU A') and empty cage controls indicated a similar inflammatory response that turned toward resolution by 14 days postimplantation, thus confirming the applicability of the cage-implant system in mice. FBGC kinetic analysis showed that the formation of mouse FBGCs occurs through the fusion of adherent macrophages at a constant rate up to 14 days of implantation. Purified goat anti-mouse IL-4 neutralizing antiBody (IL4Ab) or normal goat nonspecific control IgG (gtIgG) at various concentrations, or recombinant murine IL-4 (muIL4) was injected into the implanted cages containing PEUU A' every 2 days for 7 days. The injection of IL4Ab significantly decreased the FBGC density on PEUU A' cage-implanted in mice, when compared with the nonspecific IgG or PBS injection controls. Conversely, the FBGC density was significantly increased by the injection of muIL4 when compared with nonspecific IgG and PBS injection controls. Adherent macrophage density, FBGC morphology, FBGC average size, and size distribution were not significantly different among IL4Ab, nonspecific control gtIgG, muIL4, and PBS control groups. Our data suggest that IL-4 participates in FBGC formation on biomaterials in vivo. © 1995 John Wiley & Sons, Inc.
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role for interleukin 4 in foreign Body Giant Cell formation on a poly etherurethane urea in vivo
Journal of Biomedical Materials Research, 1995Co-Authors: Weiyuan John Kao, Amy K. Mcnally, Anne Hiltner, James M. AndersonAbstract:Interleukin-4 (IL-4) was previously shown to induce extensive macrophage fusion to form foreign-Body Giant Cells (FBGCs) in vitro. In the present study, our goal was to extend these findings to an in vivo test environment on biomaterials. The subcutaneous cage-implant system was modified for mice to elucidate IL-4 participation in mediating FBGC formation in vivo. Exudate leukocyte concentrations from cages containing poly(etherurethane urea) (PEUU A') and empty cage controls indicated a similar inflammatory response that turned toward resolution by 14 days postimplantation, thus confirming the applicability of the cage-implant system in mice. FBGC kinetic analysis showed that the formation of mouse FBGCs occurs through the fusion of adherent macrophages at a constant rate up to 14 days of implantation. Purified goat anti-mouse IL-4 neutralizing antiBody (IL4Ab) or normal goat nonspecific control IgG (gtIgG) at various concentrations, or recombinant murine IL-4 (muIL4) was injected into the implanted cages containing PEUU A' every 2 days for 7 days. The injection of IL4Ab significantly decreased the FBGC density on PEUU A' cage-implanted in mice, when compared with the nonspecific IgG or PBS injection controls. Conversely, the FBGC density was significantly increased by the injection of muIL4 when compared with nonspecific IgG and PBS injection controls. Adherent macrophage density, FBGC morphology, FBGC average size, and size distribution were not significantly different among IL4Ab, nonspecific control gtIgG, muIL4, and PBS control groups. Our data suggest that IL-4 participates in FBGC formation on biomaterials in vivo.
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Role for interleukin‐4 in foreign‐Body Giant Cell formation on a poly(etherurethane urea) in vivo
Journal of biomedical materials research, 1995Co-Authors: Weiyuan John Kao, Amy K. Mcnally, Anne Hiltner, James M. AndersonAbstract:Interleukin-4 (IL-4) was previously shown to induce extensive macrophage fusion to form foreign-Body Giant Cells (FBGCs) in vitro. In the present study, our goal was to extend these findings to an in vivo test environment on biomaterials. The subcutaneous cage-implant system was modified for mice to elucidate IL-4 participation in mediating FBGC formation in vivo. Exudate leukocyte concentrations from cages containing poly(etherurethane urea) (PEUU A') and empty cage controls indicated a similar inflammatory response that turned toward resolution by 14 days postimplantation, thus confirming the applicability of the cage-implant system in mice. FBGC kinetic analysis showed that the formation of mouse FBGCs occurs through the fusion of adherent macrophages at a constant rate up to 14 days of implantation. Purified goat anti-mouse IL-4 neutralizing antiBody (IL4Ab) or normal goat nonspecific control IgG (gtIgG) at various concentrations, or recombinant murine IL-4 (muIL4) was injected into the implanted cages containing PEUU A' every 2 days for 7 days. The injection of IL4Ab significantly decreased the FBGC density on PEUU A' cage-implanted in mice, when compared with the nonspecific IgG or PBS injection controls. Conversely, the FBGC density was significantly increased by the injection of muIL4 when compared with nonspecific IgG and PBS injection controls. Adherent macrophage density, FBGC morphology, FBGC average size, and size distribution were not significantly different among IL4Ab, nonspecific control gtIgG, muIL4, and PBS control groups. Our data suggest that IL-4 participates in FBGC formation on biomaterials in vivo.
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Theoretical analysis of in vivo macrophage adhesion and foreign Body Giant Cell formation on strained poly(etherurethane urea) elastomers.
Journal of Biomedical Materials Research, 1994Co-Authors: Weiyuan John Kao, James M. Anderson, Anne Hiltner, Gary A. LodoenAbstract:Quantitative description of foreign Body Giant Cell (FBGC) formation on poly(etherurethane urea) (PEUU) surfaces as a function of time can conceivably predict the effects of polymer characteristics on Cellular responses in vivo. In the present study, the formation of FBGCs on strained and unstrained PEUUs was quantified with two parameters: the density of adherent macrophages present initially that participate in FBGC formation (d(o)) and the rate constant for Cell fusion (k); both kinetic parameters were used to calculate the time-dependent FBGC density (dfc). Relationships were sought between results of the Cellular analysis and the extent of environmental stress cracking (ESC), as characterized by scanning electron microscopy. Surface degradation was semiquantified with percent light transmittance. The materials used were: base PEUU, base PEUU with 1% Santowhite antioxidant powder, base PEUU with 5% Methacrol 2138F antifume agent, and base PEUU with both 1% Santowhite and 5% Methacrol 2138F. A comparison of unstrained base PEUU with base PEUU strained to 400% elongation indicated that the rate of Cell fusion, but not d(o) and dfc, increased in the presence of strain. In all strained samples, additives that strongly affected the ESC also influenced FBGC kinetic parameters. Strained PEUU containing Santowhite had the lowest d(o), the slowest rate of Cell fusion, and lowest dfc, and the least incidence of ESC. The results suggest that the incidence of ESC in PEUU was decreased in the presence of Santowhite, which also lowered the number of adherent macrophages participating in FBGC formation, the rate of FBGC formation and the subsequent FBGC density. These studies also indicate that strain in PEUUs does not directly modulate the adherent macrophage and FBGC density. Further studies are necessary to delineate the relationship between PEUU strain and adherent macrophage and FBGC activation, which leads to the exocytosis of degrading agents and the observed incidence of biodegradation.
Erica Colton - One of the best experts on this subject based on the ideXlab platform.
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Paracrine and juxtacrine lymphocyte enhancement of adherent macrophage and foreign Body Giant Cell activation.
Journal of Biomedical Materials Research Part A, 2009Co-Authors: David T. Chang, Erica Colton, James M. AndersonAbstract:Lymphocytes have been shown to be involved in modulating monocyte and macrophage behavior in the foreign Body reaction. Lymphocyte effects on biomaterial-adherent macrophage and foreign Body Giant Cell (FBGC) behavior were further investigated by culturing monocytes alone or together with lymphocytes, either in direct co-cultures or indirectly in transwells, on a series of polyethylene terephthalate (PET)-based photograft co-polymerized material surfaces displaying distinct hydrophobic, hydrophilic/neutral, hydrophilic/anionic, and hydrophilic/cationic chemistries. After periods of 3, 7, and 10 days, cytokine production was quantified by ELISA and normalized to adherent macrophage/FBGC density to yield a measure of adherent macrophage/FBGC activation. Interactions with lymphocytes enhanced adherent macrophage and FBGC production of pro-inflammatory IL-1β, TNF-α, IL-6, IL-8, and MIP-1β on the hydrophobic and hydrophilic/cationic surfaces but had no effect on anti-inflammatory IL-10 production indicating lymphocytes promote a pro-inflammatory response to biomaterials. Lymphocytes also did not significantly influence MMP-9, TIMP-1, and TIMP-2 production. Interactions through indirect (paracrine) signaling showed a significant effect in enhancing adherent macrophage/FBGC activation at early time points while interactions via direct (juxtacrine) mechanisms dominated at later time points. Biomaterial surface chemistries differentially affected the observed responses as hydrophilic/neutral and hydrophilic/anionic surfaces evoked the highest levels of activation relative to the other surfaces but did not facilitate lymphocyte enhancement of adherent macrophage/FBGC activation.
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Vitronectin is a critical protein adhesion substrate for IL-4-induced foreign Body Giant Cell formation.
Journal of Biomedical Materials Research Part A, 2008Co-Authors: Amy K. Mcnally, Jacqueline A. Jones, Sarah R. Macewan, Erica Colton, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced foreign Body Giant Cell (FBGC) formation was utilized to define the adhesion protein substrate(s) that promotes this aspect of the foreign Body reaction on biomedical polymers. Human monocytes were cultured on Cell culture polystyrene surfaces that had been pre-adsorbed with a synthetic arginine-glycine-aspartate peptide previously found to support optimal FBGC formation, or with various concentrations of potential physiological protein substrates, i.e. complement C3bi, collagen types I or IV, fibrinogen, plasma fibronectin, fibroblast fibronectin, laminin, thrombospondin, vitronectin, or von Willebrand factor. Cultures were evaluated on days 0 (1.5 h), 3, and 7 by May-Grunwald/Giemsa staining. Initial monocyte adhesion occurred on all adsorbed proteins. However, by day 7 of culture, only vitronectin was striking in its ability to support significant macrophage adhesion, development, and fusion leading to FBGC formation. Vitronectin supported high degrees of FBGC formation at an absorption concentration between 5 and 25 microg/mL. These findings suggest that adsorbed vitronectin is critical in the collective events that support and promote FBGC formation on biomedical polymers, and that the propensity for vitronectin adsorption may underlie the material surface chemistry dependency of FBGC formation.
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vitronectin is a critical protein adhesion substrate for il 4 induced foreign Body Giant Cell formation
Journal of Biomedical Materials Research Part A, 2008Co-Authors: Amy K. Mcnally, Jacqueline A. Jones, Sarah R. Macewan, Erica Colton, James M. AndersonAbstract:An in vitro system of interleukin (IL)-4-induced foreign Body Giant Cell (FBGC) formation was utilized to define the adhesion protein substrate(s) that promotes this aspect of the foreign Body reaction on biomedical polymers. Human monocytes were cultured on Cell culture polystyrene surfaces that had been pre-adsorbed with a synthetic arginine-glycine-aspartate peptide previously found to support optimal FBGC formation, or with various concentrations of potential physiological protein substrates, i.e. complement C3bi, collagen types I or IV, fibrinogen, plasma fibronectin, fibroblast fibronectin, laminin, thrombospondin, vitronectin, or von Willebrand factor. Cultures were evaluated on days 0 (1.5 h), 3, and 7 by May–Grunwald/Giemsa staining. Initial monocyte adhesion occurred on all adsorbed proteins. However, by day 7 of culture, only vitronectin was striking in its ability to support significant macrophage adhesion, development, and fusion leading to FBGC formation. Vitronectin supported high degrees of FBGC formation at an absorption concentration between 5 and 25 μg/mL. These findings suggest that adsorbed vitronectin is critical in the collective events that support and promote FBGC formation on biomedical polymers, and that the propensity for vitronectin adsorption may underlie the material surface chemistry dependency of FBGC formation. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2008
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Spatial regulation and surface chemistry control of monocyte/macrophage adhesion and foreign Body Giant Cell formation by photochemically micropatterned surfaces.
Journal of Biomedical Materials Research, 1999Co-Authors: Kristin M Defife, Erica Colton, Yasuhide Nakayama, Takehisa Matsuda, James M. AndersonAbstract:A long-standing goal of biomedical device development has been the generation of specific, desired host blood and tissue responses. An approach to meeting this design criteria is precise surface modification that creates micropatterns of distinct physicochemical character to direct Cell adhesion and behavior. For this study, poly(ethylene terephthalate) films were coated with poly(benzyl N,N-diethyldithiocarbamate-co-styrene) and sequentially exposed to monomer solutions for photoirradiation. A photomask was placed over different regions to generate micropatterned surfaces with graft polymer stripes of three distinct ionic characters. Human monocytes were cultured on these surfaces to ascertain whether adhesion and fusion of monocytes/macrophages could be controlled. Nonionic polyacrylamide greatly inhibited adhesion and induced clumping of the few monocytes that did adhere. Macrophage adhesion and spreading led to high degrees of interleukin-13 induced foreign Body Giant Cell formation on both the anionic poly(acrylic acid), sodium salt, and benzyl N,N-diethyldithiocarbamate portions of the culture surface. In spite of the highest observed levels of monocyte/macrophage adhesion on cationic poly(dimethylaminopropylacrylamide), methiodide, the adherent Cells were not competent to undergo fusion to form foreign Body Giant Cells. These results suggest that inflammatory Cell responses may be spatially controlled in a manner that may be ultimately exploited to improve the biocompatibility of medical devices. © 1999 John Wiley & Sons, Inc. J Biomed Mater Res, 45, 148–154, 1999.
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spatial regulation and surface chemistry control of monocyte macrophage adhesion and foreign Body Giant Cell formation by photochemically micropatterned surfaces
Journal of Biomedical Materials Research, 1999Co-Authors: Kristin M Defife, Erica Colton, Yasuhide Nakayama, Takehisa Matsuda, James M. AndersonAbstract:A long-standing goal of biomedical device development has been the generation of specific, desired host blood and tissue responses. An approach to meeting this design criteria is precise surface modification that creates micropatterns of distinct physicochemical character to direct Cell adhesion and behavior. For this study, poly(ethylene terephthalate) films were coated with poly(benzyl N,N-diethyldithiocarbamate-co-styrene) and sequentially exposed to monomer solutions for photoirradiation. A photomask was placed over different regions to generate micropatterned surfaces with graft polymer stripes of three distinct ionic characters. Human monocytes were cultured on these surfaces to ascertain whether adhesion and fusion of monocytes/macrophages could be controlled. Nonionic polyacrylamide greatly inhibited adhesion and induced clumping of the few monocytes that did adhere. Macrophage adhesion and spreading led to high degrees of interleukin-13 induced foreign Body Giant Cell formation on both the anionic poly(acrylic acid), sodium salt, and benzyl N,N-diethyldithiocarbamate portions of the culture surface. In spite of the highest observed levels of monocyte/macrophage adhesion on cationic poly(dimethylaminopropylacrylamide), methiodide, the adherent Cells were not competent to undergo fusion to form foreign Body Giant Cells. These results suggest that inflammatory Cell responses may be spatially controlled in a manner that may be ultimately exploited to improve the biocompatibility of medical devices. © 1999 John Wiley & Sons, Inc. J Biomed Mater Res, 45, 148–154, 1999.
Christopher R. Jenney - One of the best experts on this subject based on the ideXlab platform.
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Alkylsilane-modified surfaces: inhibition of human macrophage adhesion and foreign Body Giant Cell formation.
Journal of Biomedical Materials Research, 1999Co-Authors: Christopher R. Jenney, James M. AndersonAbstract:A homologous set of alkylsilane-modified glass surfaces with chain lengths ranging from methyl to octadecyl was prepared in order to examine the influence of alkyl surface chemistry on macrophage adhesion and foreign Body Giant Cell (FBGC) formation. Contact angle and X-ray photoelectron spectroscopy analysis confirmed our silanation technique and indicated a consistent alkyl chain density independent of chain length. Human peripheral blood monocytes were isolated and cultured on these alkylsilane surfaces for a period of 10 days. The initial density of human monocytes was similar on all surfaces. Beyond day 0 the clean glass, methyl (DM and C1), propyl (C3), and hexyl (C6) surfaces maintained a high Cell density and supported macrophage development. In contrast, long-term macrophage density was extremely low on the tetradecyl (C14) and octadecyl (C18) surfaces. When interleukin-4 was added to induce FBGC formation in vitro, the DM, C1, C3, and C6 surfaces supported high levels of macrophage fusion while clean glass strongly inhibited fusion. The C14 and C18 surfaces did not contain sufficient macrophages to support FBGC formation. Cage implant studies revealed that in vivo macrophage density and FBGC formation on clean glass and C6 surfaces was similar to in vitro data. In contrast to the monocyte culture results, the C18 cage implant samples supported significant FBGC formation, possibly as a result of different conditions within each experimental system. Radiotracer adsorption studies of eight human serum proteins identified the high concentration and tenacious hold of adsorbed von Willebrand factor as being possibly involved in the poor long-term macrophage density observed on C14 and C18.
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Effects of surface-coupled polyethylene oxide on human macrophage adhesion and foreign Body Giant Cell formation in vitro.
Journal of Biomedical Materials Research, 1999Co-Authors: Christopher R. Jenney, James M. AndersonAbstract:Surface immobilized polyethylene oxide (PEO) has been shown to efficiently reduce protein adsorption and Cellular adhesion, resulting in a biologically passive surface. To explore the in vitro effects of surface immobilized PEO on the human inflammatory Cells, macrophages, and foreign Body Giant Cells (FBGCs), we developed a diisocyanate-based method for coupling PEO to amine-modified glass, a surface previously shown to enhance macrophage adhesion and FBGC formation. Contact angle analysis and X-ray photoelectron spectroscopy confirmed the presence of PEO molecules bound to the surface and revealed that PEO molecular weight significantly influenced the efficiency of PEO coupling. We used a 10-day human monocyte culture protocol to demonstrate that the presence of surface coupled PEO molecules does not significantly decrease initial monocyte density or monocyte-derived macrophage density after 3 days. However, PEO-coupled surfaces significantly reduced long-term monocyte-derived macrophage density and virtually eliminated interleukin-4-induced FBGC formation observed at day 10. The Cellular response to these PEO-coupled surfaces was related to the molecular weight of the PEO chains, which was varied between 200 Da and 18.5 kDa. These results suggest that an optimized PEO surface treatment may be effective in reducing inflammatory Cell adhesion and possible degradation during the inflammatory response to an implanted biomedical device.
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Human monocyte/macrophage adhesion, macrophage motility, and IL-4-induced foreign Body Giant Cell formation on silane-modified surfaces in vitro
Journal of Biomedical Materials Research, 1998Co-Authors: Christopher R. Jenney, Kristin M Defife, Erica Colton, James M. AndersonAbstract:A cytokine-based, in vitro model of foreign Body Giant Cell (FBGC) formation was utilized to examine the effect of biomaterial surface chemistry on the adhesion, motility, and fusion of monocytes and macrophages. Human monocytes were cultured for 10 days on 14 different silane-modified glass surfaces, during which time the Cells assumed the macrophage phenotype. The adhesion of monocytes and macrophages during the culture period decreased by an average of ∼50%, with the majority of Cell loss observed during days 1–3. Most important, the adhesion of monocytes and macrophages was surface independent except for two surfaces containing terminal methyl groups, which decreased adhesion levels. Interleukin-4 (IL-4) and granulocyte–macrophage colony-stimulating factor (GM-CSF) were added to the medium to induce FBGC formation and enhance macrophage adhesion, respectively. Surprisingly, GM-CSF decreased long-term monocyte/macrophage adhesion. IL-4-induced FBGC density was strongly influenced by the surface carbon content, as determined by X-ray photoelectron spectroscopy (XPS). In contrast, contact angle and surface energy displayed no correlation with FBGC formation. The motility of adherent macrophages, as measured by time-lapse confocal microscopy, was not affected significantly by differences in surface chemistry or the addition of cytokines. The surface dependence of FBGC formation is hypothesized to be the result of varying levels of silane-derived surface carbon. © 1998 John Wiley & Sons, Inc. J Biomed Mater Res, 41, 171–184, 1998.
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human monocyte macrophage adhesion macrophage motility and il 4 induced foreign Body Giant Cell formation on silane modified surfaces in vitro
Journal of Biomedical Materials Research, 1998Co-Authors: Christopher R. Jenney, Kristin M Defife, Erica Colton, James M. AndersonAbstract:A cytokine-based, in vitro model of foreign Body Giant Cell (FBGC) formation was utilized to examine the effect of biomaterial surface chemistry on the adhesion, motility, and fusion of monocytes and macrophages. Human monocytes were cultured for 10 days on 14 different silane-modified glass surfaces, during which time the Cells assumed the macrophage phenotype. The adhesion of monocytes and macrophages during the culture period decreased by an average of approximately 50%, with the majority of Cell loss observed during days 1-3. Most important, the adhesion of monocytes and macrophages was surface independent except for two surfaces containing terminal methyl groups, which decreased adhesion levels. Interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were added to the medium to induce FBGC formation and enhance macrophage adhesion, respectively. Surprisingly, GM-CSF decreased long-term monocyte/macrophage adhesion. IL-4-induced FBGC density was strongly influenced by the surface carbon content, as determined by X-ray photoelectron spectroscopy (XPS). In contrast, contact angle and surface energy displayed no correlation with FBGC formation. The motility of adherent macrophages, as measured by time-lapse confocal microscopy, was not affected significantly by differences in surface chemistry or the addition of cytokines. The surface dependence of FBGC formation is hypothesized to be the result of varying levels of silane-derived surface carbon.
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Human monocyte/macrophage adhesion, macrophage motility, and IL‐4‐induced foreign Body Giant Cell formation on silane‐modified surfaces in vitro
Journal of biomedical materials research, 1998Co-Authors: Christopher R. Jenney, Kristin M Defife, Erica Colton, James M. AndersonAbstract:A cytokine-based, in vitro model of foreign Body Giant Cell (FBGC) formation was utilized to examine the effect of biomaterial surface chemistry on the adhesion, motility, and fusion of monocytes and macrophages. Human monocytes were cultured for 10 days on 14 different silane-modified glass surfaces, during which time the Cells assumed the macrophage phenotype. The adhesion of monocytes and macrophages during the culture period decreased by an average of approximately 50%, with the majority of Cell loss observed during days 1-3. Most important, the adhesion of monocytes and macrophages was surface independent except for two surfaces containing terminal methyl groups, which decreased adhesion levels. Interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were added to the medium to induce FBGC formation and enhance macrophage adhesion, respectively. Surprisingly, GM-CSF decreased long-term monocyte/macrophage adhesion. IL-4-induced FBGC density was strongly influenced by the surface carbon content, as determined by X-ray photoelectron spectroscopy (XPS). In contrast, contact angle and surface energy displayed no correlation with FBGC formation. The motility of adherent macrophages, as measured by time-lapse confocal microscopy, was not affected significantly by differences in surface chemistry or the addition of cytokines. The surface dependence of FBGC formation is hypothesized to be the result of varying levels of silane-derived surface carbon.