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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 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
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.
J M Anderson - One of the best experts on this subject based on the ideXlab platform.
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Protein-mediated macrophage adhesion and activation on biomaterials: a model for modulating Cell behavior
Journal of Materials Science: Materials in Medicine, 1999Co-Authors: J M AndersonAbstract:The elucidation of proteins involved in biomaterial-modulated macrophage behavior is critical for the improvement of material performance and the initial exploration of material design capable of manipulating macrophage function for tissue engineering. In this paper, several in vitro and in vivo techniques are presented to demonstrate means of delineating a part of the complex molecular mechanisms involved in the interaction between biomaterial and macrophage adhesion and phenotypic development. The following conclusions were reached: (1) using radioimmunoassay, complement component C3 was found to be critical in mediating human macrophage adhesion on polyurethanes. (2) The presence of a diphenolic antioxidant additive in polyurethanes increased the propensity for complement upregulation but did not affect adherent macrophage density. (3) The subcutaneous cage-implant system was utilized to delineate interleukin-4 participation in the fusion of adherent macrophages to form foreign body Giant Cells in vivo in mice. The injection of purified interleukin-4 neutralizing antibody into the implanted cages significantly decreased the Giant Cell density; conversely, the Giant Cell density was significantly increased by the injection of recombinant interleukin-4 when compared with the controls. (4) The RGD and PHSRN amino acid sequences of the central Cell binding domain and the PRRARV sequence of the C-terminal heparin binding domain of human plasma fibronectin were utilized to study the structure-functional relationship of protein in mediating macrophage behavior. Polyethyleneglycol-based networks grafted with the RGD-containing peptide supported higher adherent human macrophage density than surfaces grafted with other peptides. The formation of foreign body Giant Cell was highly dependent on the relative orientation between PHSRN and RGD domains located in a single peptide. © 1999 Kluwer Academic Publishers
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Monocyte, macrophage and foreign body Giant Cell interactions with molecularly engineered surfaces
Journal of Materials Science: Materials in Medicine, 1999Co-Authors: J M Anderson, K. Defife, A. Mcnally, T. Collier, C. JenneyAbstract:To elucidate the mechanisms involved in monocyte/macrophage adhesion and fusion to form foreign body Giant Cells on molecularly engineered surfaces, we have utilized our in vitro culture system to examine surface chemistry effects, cytoskeletal reorganization and adhesive structure development, and Cell receptor-ligand interactions in in vitro foreign body Giant Cell formation. Utilizing silane-modified surfaces, monocyte/macrophage adhesion was essentially unaffected by surface chemistry, however the density of foreign body Giant Cells (FBGCs) was correlated with surface carbon content. An exception to the surface-independent macrophage adhesion were the alkyl-silane modified surfaces which exhibited reduced adhesion and FBGC formation. Utilizing confocal immunofluorescent techniques, cytoskeletal reorganization and adhesive structure development in in vitro FBGC formation was studied. Podosomes were identified as the adhesive structures in macrophages and FBGCs based on the presence of characteristic cytoplasmic proteins and F-actin at the ventral Cell surface. Focal adhesion kinase (FAK) and focal adhesions were not identified as the adhesive structures in macrophages and FBGCs. In studying the effect of preadsorbed proteins on FBGC formation, fibronectin or vitronectin do not play major roles in initial monocyte/macrophage adhesion, whereas polystyrene surfaces modified with RGD exhibited significant FBGC formation. These studies identify the potential importance of surface chemistry-dependent conformational alterations which may occur in proteins adsorbed to surfaces and their potential involvement in receptor-ligand interactions. Significantly, preadsorption of α_2-macroglobulin facilitated macrophage fusion and FBGC formation readily on the RGD surface in the absence of any additional serum proteins. As α_2-macroglobulin receptors are not found on blood monocytes but are expressed only with macrophage development, these results point to a potential interaction between adsorbed α_2-macroglobulin and its receptors on macrophages during macrophage development and fusion. These studies identify important surface independent and dependent effects in foreign body reaction development that may be important in the identification of biological design criteria for molecularly engineered surfaces and tissue engineered devices. © 1999 Kluwer Academic Publishers
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Monocyte, macrophage and foreign body Giant Cell interactions with molecularly engineered surfaces.
Journal of materials science. Materials in medicine, 1999Co-Authors: J M Anderson, K. Defife, A. Mcnally, T. Collier, C. JenneyAbstract:To elucidate the mechanisms involved in monocyte/macrophage adhesion and fusion to form foreign body Giant Cells on molecularly engineered surfaces, we have utilized our in vitro culture system to examine surface chemistry effects, cytoskeletal reorganization and adhesive structure development, and Cell receptor-ligand interactions in in vitro foreign body Giant Cell formation. Utilizing silane-modified surfaces, monocyte/macrophage adhesion was essentially unaffected by surface chemistry, however the density of foreign body Giant Cells (FBGCs) was correlated with surface carbon content. An exception to the surface-independent macrophage adhesion were the alkyl-silane modified surfaces which exhibited reduced adhesion and FBGC formation. Utilizing confocal immunofluorescent techniques, cytoskeletal reorganization and adhesive structure development in in vitro FBGC formation was studied. Podosomes were identified as the adhesive structures in macrophages and FBGCs based on the presence of characteristic cytoplasmic proteins and F-actin at the ventral Cell surface. Focal adhesion kinase (FAK) and focal adhesions were not identified as the adhesive structures in macrophages and FBGCs. In studying the effect of preadsorbed proteins on FBGC formation, fibronectin or vitronectin do not play major roles in initial monocyte/macrophage adhesion, whereas polystyrene surfaces modified with RGD exhibited significant FBGC formation. These studies identify the potential importance of surface chemistry-dependent conformational alterations which may occur in proteins adsorbed to surfaces and their potential involvement in receptor-ligand interactions. Significantly, preadsorption of alpha2-macroglobulin facilitated macrophage fusion and FBGC formation readily on the RGD surface in the absence of any additional serum proteins. As alpha2-macroglobulin receptors are not found on blood monocytes but are expressed only with macrophage development, these results point to a potential interaction between adsorbed 2-macroglobulin and its receptors on macrophages during macrophage development and fusion. These studies identify important surface independent and dependent effects in foreign body reaction development that may be important in the identification of biological design criteria for molecularly engineered surfaces and tissue engineered devices.
D. A. Foschi - One of the best experts on this subject based on the ideXlab platform.
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Tissue response to polyester mesh for hernia repair: An ultramicroscopic study in man
Hernia, 1998Co-Authors: E. E. Trabucchi, F. R. Corsi, C. Meinardi, P. Cellerino, R. Allevi, D. A. FoschiAbstract:We studied by ultramicroscopy the tissue response after mesh hernia repair. 11 patients, bearing dacron mesh from 7 days to 9 years, were biopsied during later operations. There were two groups of patients: 6 with a normal tissue response and 5 with rejection of the mesh. We observed that mesh repair was characterised by development of a Foreign-Body Giant Cell layer around the fibres, the presence of macrophages in an intermediate layer and fibroblasts in the outer layer. Collagen fibres and bundles ran between the Giant Cells and the host tissues. When the mesh was rejected, there were no chronic inflammatory Cells and collagen bundles were reabsorbed. In the peripheral areas where the mesh-integrated tissue still persisted, there was a considerable reduction in the numbers of the Giant Cells and there were red blood Cells and acute inflammatory Cells instead of macrophages and epithelioid Cells. Collagen was reduced to fibrils. From our results, mesh-tissue repair seems to be a dynamic and unstable process characterised by chronic inflammation and continuous collagen maturation. During the development, the tissue response to the mesh, as with any inflammatory condition, makes colorisation by hematogenic bacteria easier. Infection can destroy the capsule around the mesh and causes its rejection.
Thomas A Horbett - One of the best experts on this subject based on the ideXlab platform.
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effects of adsorbed proteins and surface chemistry on foreign body Giant Cell formation tumor necrosis factor alpha release and procoagulant activity of monocytes
Journal of Biomedical Materials Research Part A, 2004Co-Authors: Mingchao Shen, Iris Garcia, Ronald V Maier, Thomas A HorbettAbstract:The adhesion and activation of monocytes and macrophages are thought to affect the foreign body response to implanted medical devices. However, these Cells interact with devices indirectly, because of the prior adsorption of proteins. Therefore, we preadsorbed several “model” biomaterial surfaces with proteins and then measured foreign body Giant Cell (FBGC) formation, tumor necrosis factor alpha (TNFα) release, and procoagulant activity. The model surfaces were tissue culture polystyrene (TCPS), untreated polystyrene (PS), and Primaria, whereas the proteins used were albumin, fibronectin, fibrinogen, and immunoglobulin. FBGC formation, TNFα release, and procoagulant activity of monocytes were the highest for surfaces preadsorbed with IgG. FBGC formation was lower on surfaces with adsorbed fibrinogen and fibronectin than on uncoated surfaces. TNFα release and procoagulant activity of monocytes were similar on surface adsorbed with fibrinogen, fibronectin, or albumin. Monocyte activation was also affected by the surface chemistry of the substrates, because FBGC formation was the highest on PS and the lowest on TCPS. Monocyte procoagulant activity was the highest on Primaria. Adsorbed proteins and surface chemistry were found to have strong effects on FBGC formation, monocyte TNFα release, and procoagulant activity in vitro, providing support for the idea that these same variables could affect macrophage-mediated foreign body response to biomaterials in vivo. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res 70A: 533–541, 2004