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James M. Anderson - One of the best experts on this subject based on the ideXlab platform.

  • Evaluation of clinical Biomaterial Surface effects on T lymphocyte activation
    Journal of biomedical materials research. Part A, 2010
    Co-Authors: Analiz Rodriguez, James M. Anderson
    Abstract:

    Previous in vitro studies in our laboratory have shown that lymphocytes can influence macrophage adhesion and fusion on Biomaterial Surfaces. However, few studies have evaluated how material adherent macrophages can influence lymphocyte behavior, specifically T cells. In this study, we cultured human peripheral blood mononuclear cells from healthy donors on three synthetic nonbiodegradable biomedical polymers: elasthane 80A (PEU), silicone rubber (SR), or polyethylene terephthalate (PET) and tissue culture polystyrene (TCPS). Upregulation of T cell Surface activation markers (CD69 and CD25), lymphocyte proliferation, and interleukin-2 (IL-2) and interferon-gamma (IFNgamma) concentrations were evaluated by flow cytometry, carboxy-fluorescein diacetate, succinimydyl ester (CFSE) incorporation, and multiplex cytokine immunoassay, respectively, to assess T cell activation. Following 3 and 7 days of culture, CD4+ helper T cells from cultures of any of the material groups did not express the activation markers CD69 and CD25 and lymphocyte proliferation was not present. IL-2 and IFNgamma levels were produced, but dependent on donor. These data indicate that T cells are not activated in response to clinically relevant synthetic Biomaterials. The data also suggest that lymphocyte subsets exclusive of T cells are the source of the lymphokines, IL-2 and IFN-gamma, in certain donors.

  • Lymphocyte adhesion and interactions with Biomaterial adherent macrophages and foreign body giant cells.
    Journal of Biomedical Materials Research Part A, 2009
    Co-Authors: David T Chang, Erica Colton, Takehisa Matsuda, James M. Anderson
    Abstract:

    To characterize the effects of adherent macrophages and Biomaterial Surface chemistries on lymphocyte adhesion and activation, lymphocytes were co-cultured with monocytes alone and together, directly and separated by a porous membrane transwell on hydrophobic, hydrophilic/neutral, hydrophilic/anionic, and hydrophilic/cationic Biomaterial Surfaces. Surface adherent cells were quantitatively analyzed after 3 days utilizing immunofluorescence and phase contrast imaging. After periods of 3, 7, and 10 days, secreted interferon-γ (IFN-γ) was quantified by ELISA. Limited direct Biomaterial-adherent lymphocytes were identified regardless of the presence of macrophages or foreign body giant cells (FBGC). The majority of adherent lymphocytes, which were T cells (> 95%) rather than natural killer cells, predominantly interacted with adherent macrophages and FBGCs; greater than 90% were interacting on Surfaces with higher levels of adherent macrophages and FBGCs and greater than 55% were interacting on Surfaces with lower levels of macrophages and FBGCs. The hydrophilic/anionic Surface promoted higher levels of macrophage- and FBGC-adherent lymphocytes but was nonselective for lymphocyte subtype interactions. The hydrophilic/neutral Surface was selective for CD4+ T lymphocyte interactions while the hydrophobic Surface was selective for CD8+ T lymphocyte interactions. IFN-γ was produced in direct and indirect co-cultures but not in lymphocyte- and monocyte-only cultures suggesting that lymphocytes are activated via macrophage-derived cytokines rather than direct Biomaterial contact. Direct lymphocyte interactions with adherent macrophages/FBGCs enhanced IFN-γ production relative to indirect co-cultures. These results suggest that lymphocytes prefer interactions with adherent macrophages and FBGCs, resulting in lymphocyte activation, and these interactions can be influenced by Biomaterial Surface chemistries.

  • In Vitro and In Vivo Monocyte, Macrophage, Foreign Body Giant Cell, and Lymphocyte Interactions with Biomaterials
    Biological Interactions on Materials Surfaces, 2009
    Co-Authors: James M. Anderson
    Abstract:

    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.

  • lymphocyte macrophage interactions Biomaterial Surface dependent cytokine chemokine and matrix protein production
    Journal of Biomedical Materials Research Part A, 2008
    Co-Authors: David T Chang, Takehisa Matsuda, Erica Colton, Jacqueline A Jones, Howard J Meyerson, Il Keun Kwon, James M. Anderson
    Abstract:

    The role of lymphocytes in the biological response to synthetic polymers is poorly understood despite the transient appearance of lymphocytes at the Biomaterial implant site. To investigate cytokines, chemokines, and extracellular matrix (ECM) proteins produced by lymphocytes and macrophages in response to Biomaterial Surfaces, human peripheral blood monocytes and lymphocytes were co-cultured on polyethylene terephthalate (PET)-based material Surfaces displaying distinct hydrophobic, hydrophilic/neutral, hydrophilic/anionic, and hydrophilic/cationic chemistries. Antibody array screening showed the majority of detected proteins are inflammatory mediators that guide the early inflammatory phases of wound healing. Proteomic ELISA quantification and adherent cell analysis were performed after 3, 7, and 10 days of culture. IL-2 and IFN-γ were not detected in any co-cultures suggesting lack of lymphocyte activation. The hydrophilic/neutral Surfaces increased IL-8 relative to the hydrophobic PET Surface (p<0.05). The hydrophilic/anionic Surfaces promoted increased TNF-α over hydrophobic and cationic Surfaces and increased MIP-1β compared to hydrophobic Surfaces (p<0.05). Since enhanced macrophage fusion was observed on hydrophilic/anionic Surfaces, the production of these cytokines likely plays an important role in the fusion process. The hydrophilic/cationic Surface promoted IL-10 production and increased matrix metalloproteinase (MMP)-9/tissue inhibitor of MMP (TIMP) relative to hydrophilic/neutral and anionic Surfaces (p<0.05). These results suggest hydrophilic/neutral and anionic Surfaces promote pro-inflammatory responses and reduced degradation of the ECM, whereas the hydrophilic/cationic Surfaces induce an anti-inflammatory response and greater MMP-9/TIMP with an enhanced potential for ECM breakdown. The study also underscores the usefulness of protein arrays in assessing the role of soluble mediators in the inflammatory response to Biomaterials.

  • Proteomic analysis and quantification of cytokines and chemokines from Biomaterial Surface-adherent macrophages and foreign body giant cells
    Journal of Biomedical Materials Research Part A, 2007
    Co-Authors: Jacqueline A Jones, Takehisa Matsuda, Erica Colton, David T Chang, Howard J Meyerson, Il Keun Kwon, James M. Anderson
    Abstract:

    Implantation of Biomaterial devices results in the well-known foreign body reaction consisting of monocytes, macrophages, and foreign body giant cells (FBGCs) at the material/tissue interface. We continue to address the hypothesis that material Surface chemistry modulates the phenotypic expression of these cells. Utilizing our human monocyte culture system, we have used Surface-modified polymers displaying hydrophobic, hydrophilic, and/or ionic chemistries to determine the cytokines/chemokines released from Biomaterial-adherent macrophages/FBGCs. This study broadens our approach by using proteomic analysis to identify important factors expressed by these cells and further quantifies these molecules with ELISAs. Proteomic profiles changed over time suggesting that the adherent macrophages underwent a phenotypic switch. Macrophage/FBGC-derived proinflammatory cytokines, IL-1β and IL-6, decreased with time, while the anti-inflammatory cytokine, IL-10, gradually increased with time. Resolution of the inflammatory response was also demonstrated by a decrease in chemoattractant IL-8 and MIP-1β production with time. Material-dependent macrophage/FBGC activation was analyzed using cytokine/chemokine production and cellular adhesion. Monocyte/macrophage adhesion was similar on all Surfaces, except for the hydrophilic/neutral Surfaces that showed a significant decrease in cellular density and minimal FBGC formation. Normalizing the ELISA data based on the adherent cell population provided cytokine/chemokine concentrations produced per cell. This analysis showed that although there were fewer cells on the hydrophilic/neutral Surface, these adherent cells were further activated to produce significantly greater amounts of each cytokine/chemokine tested than the other Surfaces. This study clearly presents evidence that material Surface chemistry can differentially affect monocyte/macrophage/FBGC adhesion and cytokine/chemokine profiles derived from activated macrophages/FBGCs adherent to Biomaterial Surfaces. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res 2007

Jasmine D Patel - One of the best experts on this subject based on the ideXlab platform.

  • s epidermidis biofilm formation effects of Biomaterial Surface chemistry and serum proteins
    Journal of Biomedical Materials Research Part A, 2007
    Co-Authors: Jasmine D Patel, Michael J Ebert, Robert Ward, James M. Anderson
    Abstract:

    Most infections due to implanted cardiovascular Biomaterials are initiated by bacterial adhesion of Staphylococcus epidermidis, followed by colonization and biofilm formation on the Surface of the implant. This study examined the role of serum proteins and material Surface chemistry in the formation of S. epidermidis biofilm on polyurethanes (Elasthane 80A, hydrophobic) modified with polyethylene oxide (Elasthane 80A-6PEO, hydrophilic) and fluorocarbon (Elasthane 80A-6F, hydrophobic). Initial adhesion, aggregation, biofilm thickness, viability, and slime formation of S. epidermidis strain, RP62A in phosphate buffered saline (PBS), tryptic soy broth (TBS), and 20% pooled human serum was quantified. In the presence of adsorbed serum proteins, initial bacterial adhesion was suppressed significantly to <2% relative to adhesion in TSB or PBS. However, adhesion, aggregation, and proliferation increased dramatically in the 12–24 h period on Elasthane 80A and Elasthane 80A-6F, which resulted in an extensive network of biofilm. A contrasting trend was observed on the hydrophilic Elasthane 80A-6PEO Surface, with minimal bacterial adhesion, which decreased steadily over 24 h. In the presence of serum proteins, an increasingly thick (∼20 μm) biofilm formed on the hydrophobic Surfaces over 48 h whereas the formation of a mature biofilm on the hydrophilic Surface was impeded with few viable bacteria present over 48 h. Furthermore, slime was detected during the initial phase of bacterial adhesion at 2 h and increased over time with the formation of biofilm. These results have shown that while initial S. epidermidis adhesion is suppressed in the presence of adsorbed proteins, inter-bacterial adhesion possibly aided by slime production leads to the formation of a robust mature biofilm. Also, Biomaterial Surface chemistry affected biofilm formation and, most notably, polyethylene oxide significantly inhibited S. epidermidis biofilm formation over 48 h in vitro. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2007

  • S. epidermidis biofilm formation: Effects of Biomaterial Surface chemistry and serum proteins
    Journal of Biomedical Materials Research Part A, 2007
    Co-Authors: Jasmine D Patel, Michael J Ebert, Robert Ward, James M. Anderson
    Abstract:

    Most infections due to implanted cardiovascular Biomaterials are initiated by bacterial adhesion of Staphylococcus epidermidis, followed by colonization and biofilm formation on the Surface of the implant. This study examined the role of serum proteins and material Surface chemistry in the formation of S. epidermidis biofilm on polyurethanes (Elasthane 80A, hydrophobic) modified with polyethylene oxide (Elasthane 80A-6PEO, hydrophilic) and fluorocarbon (Elasthane 80A-6F, hydrophobic). Initial adhesion, aggregation, biofilm thickness, viability, and slime formation of S. epidermidis strain, RP62A in phosphate buffered saline (PBS), tryptic soy broth (TBS), and 20% pooled human serum was quantified. In the presence of adsorbed serum proteins, initial bacterial adhesion was suppressed significantly to

  • effects of Biomaterial Surface chemistry on the adhesion and biofilm formation of staphylococcus epidermidis in vitro
    Journal of Biomedical Materials Research Part A, 2006
    Co-Authors: Erin E Mackintosh, Jasmine D Patel, Roger E Marchant, James M. Anderson
    Abstract:

    The formation of biofilm, a structured community of bacteria enclosed in slime, is a significant virulence factor in medical-device-centered infection. The development of cardiovascular device infection can be separated into two phases: initial bacterial adhesion and aggregation, followed by proliferation and production of slime. It is possible to modulate the adhesion and biofilm formation of Staphylococcus epidermidis, a commensal skin bacterium commonly found on infected medical devices, through Biomaterial Surface chemistry. This study examines bacterial adhesion and biofilm formation on Surface-modified polyethylene terephthalate (PET), including Surfaces with varying hydrophilic, hydrophobic, and ionic character. Bacterial adhesion and biofilm formation were observed over 48 hours in phosphate-buffered saline (PBS) and 20% pooled human serum. The hydrophilic Surface (PAAm) had significantly less nonspecific adhesion of bacteria than that in the control (PET) and other Surfaces, when cultured in PBS (P < 0.0001). Charged Surfaces, both anionic and cationic, had increased adhesion and aggregation of bacteria in comparison with the control (PET) in the presence of serum proteins over 24 hours (P < 0.0001). Bacteria cultured in serum on the charged Surfaces did not have significantly different amounts of biofilm formation compared with that of the control (PET) Surface after 48 hours. This study showed that Biomaterial Surface chemistry characteristics impact initial adhesion and aggregation of S. epidermidis on Biomaterials. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006

  • Effects of Biomaterial Surface chemistry on the adhesion and biofilm formation of Staphylococcus epidermidis in vitro.
    Journal of biomedical materials research. Part A, 2006
    Co-Authors: Erin E Mackintosh, Jasmine D Patel, Roger E Marchant, James M. Anderson
    Abstract:

    The formation of biofilm, a structured community of bacteria enclosed in slime, is a significant virulence factor in medical-device-centered infection. The development of cardiovascular device infection can be separated into two phases: initial bacterial adhesion and aggregation, followed by proliferation and production of slime. It is possible to modulate the adhesion and biofilm formation of Staphylococcus epidermidis, a commensal skin bacterium commonly found on infected medical devices, through Biomaterial Surface chemistry. This study examines bacterial adhesion and biofilm formation on Surface-modified polyethylene terephthalate (PET), including Surfaces with varying hydrophilic, hydrophobic, and ionic character. Bacterial adhesion and biofilm formation were observed over 48 hours in phosphate-buffered saline (PBS) and 20% pooled human serum. The hydrophilic Surface (PAAm) had significantly less nonspecific adhesion of bacteria than that in the control (PET) and other Surfaces, when cultured in PBS (P < 0.0001). Charged Surfaces, both anionic and cationic, had increased adhesion and aggregation of bacteria in comparison with the control (PET) in the presence of serum proteins over 24 hours (P < 0.0001). Bacteria cultured in serum on the charged Surfaces did not have significantly different amounts of biofilm formation compared with that of the control (PET) Surface after 48 hours. This study showed that Biomaterial Surface chemistry characteristics impact initial adhesion and aggregation of S. epidermidis on Biomaterials.

Kristina Nilsson Ekdahl - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of complement activation on a model Biomaterial Surface by streptococcal M protein-derived peptides.
    Biomaterials, 2009
    Co-Authors: Anna E. Engberg, Bo Nilsson, Kerstin Sandholm, Fredrik Bexborn, Jenny J. Persson, Gunnar Lindahl, Kristina Nilsson Ekdahl
    Abstract:

    The aim of this study was to evaluate a new approach to inhibit complement activation triggered by Biomaterial Surfaces in contact with blood. In order to inhibit complement activation initiated by ...

  • binding of c3 fragments on top of adsorbed plasma proteins during complement activation on a model Biomaterial Surface
    Biomaterials, 2005
    Co-Authors: Jonas Andersso, Kristina Nilsson Ekdahl, John D. Lambris, O Nilsso
    Abstract:

    In the present study we investigate whether complement activation in blood in contact with a model Biomaterial Surface (polystyrene) occurs directly on the material Surface or on top of an adsorbed plasma protein layer. Quartz crystal microbalance-dissipation analysis (QCM-D) complemented with enzyme immunoassays and Western blotting were used. QCM-D showed that the Surface was immediately covered with a plasma protein film of approximately 8 nm. Complement activation that started concomitantly with the adsorption of the protein film was triggered by a self-limiting classical pathway activation. After adsorption of the protein film, alternative pathway activation provided the bulk of the C3b deposition that added 25% more mass to the Surface. The build up of alternative pathway convertase complexes using purified C3 and factors B and D on different protein films as monitored by QCM-D showed that only adsorbed albumin, IgG, but not fibrinogen, allowed C3b binding, convertase assembly and amplification. Western blotting of eluted proteins from the material Surface demonstrated that the C3 fragments were covalently bound to other proteins. This is consistent with a model in which the activation is triggered by initiating convertases formed by means of the initially adsorbed proteins and the main C3b binding is mediated by the alternative pathway on top of the adsorbed protein film.

  • Complement activation on a model Biomaterial Surface: Binding of C3b via the alternative amplification loop to plasma proteins adsorbed to the Surface
    Biomaterials, 2003
    Co-Authors: Jonas Andersson, Kristina Nilsson Ekdahl, John D. Lambris, Bo Nilsson
    Abstract:

    Complement activation on a model Biomaterial Surface: Binding of C3b via the alternative amplification loop to plasma proteins adsorbed to the Surface

  • binding of a model regulator of complement activation rca to a Biomaterial Surface Surface bound factor h inhibits complement activation
    Biomaterials, 2001
    Co-Authors: Jonas Andersson, Rolf Larsson, R Richter, Kristina Nilsson Ekdahl, Bo Nilsson
    Abstract:

    The complement system is an important inflammatory mediator during procedures such as cardiopulmonary bypass and hemodialysis when blood is exposed to large areas of Biomaterial Surface. This contact between blood and the Biomaterials of implants and extracorporeal circuits leads to an inflammatory response mediated by the complement system. The aim of this study was to assess the ability of a complement regulator (factor H) immobilised on a Biomaterial Surface to inhibit complement cascade mediated inflammatory responses. The cross-linker N-succinimidyl 3-(2-pyridyldithio) propionate was used to immobilise factor H on a model Biomaterial Surface without affecting the biological activity of the inhibitor. Binding of factor H was then characterised using quartz crystal microbalance-dissipation (QCM-D) and enzyme immunoassays for products of complement activation: bound C3 fragments and soluble C3a, sC5b-9, and C1s-C1INA. Immobilised factor H reduced the amount C3 fragments deposited on the Biomaterial Surface after incubation with serum, plasma, or whole blood. In addition, lower levels of soluble C3a and sC5b-9 were generated after incubation with whole blood. In summary, we have demonstrated that complement activation on a highly activating model Surface can be inhibited by immobilised factor H and have defined prerequisites for the preparation of future Biomaterial Surfaces with immobilised regulators of complement activation.

Bo Nilsson - One of the best experts on this subject based on the ideXlab platform.

Roger E Marchant - One of the best experts on this subject based on the ideXlab platform.

  • effects of Biomaterial Surface chemistry on the adhesion and biofilm formation of staphylococcus epidermidis in vitro
    Journal of Biomedical Materials Research Part A, 2006
    Co-Authors: Erin E Mackintosh, Jasmine D Patel, Roger E Marchant, James M. Anderson
    Abstract:

    The formation of biofilm, a structured community of bacteria enclosed in slime, is a significant virulence factor in medical-device-centered infection. The development of cardiovascular device infection can be separated into two phases: initial bacterial adhesion and aggregation, followed by proliferation and production of slime. It is possible to modulate the adhesion and biofilm formation of Staphylococcus epidermidis, a commensal skin bacterium commonly found on infected medical devices, through Biomaterial Surface chemistry. This study examines bacterial adhesion and biofilm formation on Surface-modified polyethylene terephthalate (PET), including Surfaces with varying hydrophilic, hydrophobic, and ionic character. Bacterial adhesion and biofilm formation were observed over 48 hours in phosphate-buffered saline (PBS) and 20% pooled human serum. The hydrophilic Surface (PAAm) had significantly less nonspecific adhesion of bacteria than that in the control (PET) and other Surfaces, when cultured in PBS (P < 0.0001). Charged Surfaces, both anionic and cationic, had increased adhesion and aggregation of bacteria in comparison with the control (PET) in the presence of serum proteins over 24 hours (P < 0.0001). Bacteria cultured in serum on the charged Surfaces did not have significantly different amounts of biofilm formation compared with that of the control (PET) Surface after 48 hours. This study showed that Biomaterial Surface chemistry characteristics impact initial adhesion and aggregation of S. epidermidis on Biomaterials. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006

  • Effects of Biomaterial Surface chemistry on the adhesion and biofilm formation of Staphylococcus epidermidis in vitro.
    Journal of biomedical materials research. Part A, 2006
    Co-Authors: Erin E Mackintosh, Jasmine D Patel, Roger E Marchant, James M. Anderson
    Abstract:

    The formation of biofilm, a structured community of bacteria enclosed in slime, is a significant virulence factor in medical-device-centered infection. The development of cardiovascular device infection can be separated into two phases: initial bacterial adhesion and aggregation, followed by proliferation and production of slime. It is possible to modulate the adhesion and biofilm formation of Staphylococcus epidermidis, a commensal skin bacterium commonly found on infected medical devices, through Biomaterial Surface chemistry. This study examines bacterial adhesion and biofilm formation on Surface-modified polyethylene terephthalate (PET), including Surfaces with varying hydrophilic, hydrophobic, and ionic character. Bacterial adhesion and biofilm formation were observed over 48 hours in phosphate-buffered saline (PBS) and 20% pooled human serum. The hydrophilic Surface (PAAm) had significantly less nonspecific adhesion of bacteria than that in the control (PET) and other Surfaces, when cultured in PBS (P < 0.0001). Charged Surfaces, both anionic and cationic, had increased adhesion and aggregation of bacteria in comparison with the control (PET) in the presence of serum proteins over 24 hours (P < 0.0001). Bacteria cultured in serum on the charged Surfaces did not have significantly different amounts of biofilm formation compared with that of the control (PET) Surface after 48 hours. This study showed that Biomaterial Surface chemistry characteristics impact initial adhesion and aggregation of S. epidermidis on Biomaterials.

  • Biomaterial Surface dependent neutrophil mobility
    Journal of Biomedical Materials Research Part A, 2004
    Co-Authors: Yue Zhou, James M. Anderson, Claire M Doerschuk, Roger E Marchant
    Abstract:

    Compromised neutrophil function in the presence of an implanted Biomaterial may represent an important mechanism that allows for the development of implant-associated infections. Here, human neutrophil mobility has been investigated on a polyurethane (ChronoFlex AR), a hydrophobic Surface consisting of an octadecyltrichlorosilane (OTS) self-assembled monolayer, and a glass reference material. Neutrophil mobility was quantified, based on cell movement speed and persistence time obtained from time-lapse optical microscopy, while neutrophil cytoskeletal structures and morphology were visualized using confocal microscopy and atomic force microscopy. Our results show that material Surface properties affect neutrophil-Surface interactions, as reflected by morphological changes, and the mobility of neutrophils stimulated by N-formylmethionyl-leucyl-phenylalanine (fMLP). In the absence of adsorbed plasma proteins, the mobility of stimulated neutrophils increased with increasing material hydrophobicity from glass, to polyurethane, to OTS. The opposite trend was observed in the presence of adsorbed plasma proteins, such that neutrophil mobility increased with decreasing material hydrophobicity. Analysis of the results showed that the mobility of fMLP-stimulated neutrophils cells was inversely related to the extent of cell spreading on the materials.