The Experts below are selected from a list of 91824 Experts worldwide ranked by ideXlab platform
Liping Tang - One of the best experts on this subject based on the ideXlab platform.
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molecular basis of biomaterial mediated foreign body reactions
Blood, 2001Co-Authors: Wenjing Hu, Tatiana P Ugarova, John W. Eaton, Liping TangAbstract:Despite being inert and nontoxic, implanted Biomaterials often trigger adverse foreign body reactions such as inflammation, fibrosis, infection, and thrombosis. With regard to the inflammatory responses to biomaterial implants, it was previously found that a crucial precedent event was the spontaneous adsorption and denaturation of fibrinogen on implant surfaces. It was further found that interactions between the phagocyte integrin Mac-1 (CD11b/CD18) and one short sequence within the fibrinogen D domain (γ190-202; P1) at least partially explained phagocyte accumulation on implant surfaces. However, the reason that adsorbed fibrinogen is proinflammatory—while soluble fibrinogen clearly is not—remained obscure. In this study, therefore, the question of how fibrinogen is converted to a proinflammatory state when adsorbed to biomaterial surfaces is investigated. In soluble fibrinogen, the 13 amino acid P1 sequence was found to be hidden. However, the adsorption and denaturation of fibrinogen on the surfaces of commonly used Biomaterials lead to the exposure of P1 and a second neo-epitope, γ377-395 (P2), which also interacts with Mac-1 and is similarly occult in the soluble protein. The extent of biomaterial-mediated P1 and P2 exposure appears directly related to the severity of inflammatory responses to a test panel of Biomaterials. Finally, thrombin-mediated conversion of fibrinogen to fibrin also exposes both P1 and P2 epitopes. These observations may help explain both the inflammation caused by many types of implanted Biomaterials and that which occurs naturally following thrombotic events.
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mast cells mediate acute inflammatory responses to implanted Biomaterials
Proceedings of the National Academy of Sciences of the United States of America, 1998Co-Authors: Liping Tang, Timothy A Jennings, John W. EatonAbstract:Implanted Biomaterials trigger acute and chronic inflammatory responses. The mechanisms involved in such acute inflammatory responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, and adhesion to implant surfaces. We earlier observed that two chemokines-macrophage inflammatory protein 1alpha/monocyte chemoattractant protein 1-and the phagocyte integrin Mac-1 (CD11b/CD18)/surface fibrinogen interaction are, respectively, required for phagocyte chemotaxis and adherence to biomaterial surfaces. However, it is still not clear how the initial transmigration of phagocytes through the endothelial barrier into the area of the implant is triggered. Because implanted Biomaterials elicit histaminic responses in the surrounding tissue, and histamine release is known to promote rapid diapedesis of inflammatory cells, we evaluated the possible role of histamine and mast cells in the recruitment of phagocytes to biomaterial implants. Using i.p. and s. c. implantation of polyethylene terephthalate disks in mice we find: (i) Extensive degranulation of mast cells, accompanied by histamine release, occurs adjacent to short-term i.p. implants. (ii) Simultaneous administration of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respectively) greatly diminishes recruitment and adhesion of both neutrophils (<20% of control) and monocytes/macrophages (<30% of control) to implants. (iii) Congenitally mast cell-deficient mice also exhibit markedly reduced accumulation of phagocytes on both i.p. and s.c implants. (iv) Finally, mast cell reconstitution of mast cell-deficient mice restores "normal" inflammatory responses to biomaterial implants. We conclude that mast cells and their granular products, especially histamine, are important in recruitment of inflammatory cells to biomaterial implants. Improved knowledge of such responses may permit purposeful modulation of both acute and chronic inflammation affecting implanted Biomaterials.
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mast cells mediate acute inflammatory responses to implanted Biomaterials histamineyphagocytes
1998Co-Authors: Liping Tang, Imothy T A Jennings, John W. EatonAbstract:Implanted Biomaterials trigger acute and chronic inf lammatory responses. The mechanisms involved in such acute inf lammatory responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, and adhesion to implant surfaces. We earlier observed that two chemokines— macrophage inf lammatory protein 1aymonocyte chemoat- tractant protein 1—and the phagocyte integrin Mac-1 (CD11byCD18)ysurface fibrinogen interaction are, respec- tively, required for phagocyte chemotaxis and adherence to biomaterial surfaces. However, it is still not clear how the initial transmigration of phagocytes through the endothelial barrier into the area of the implant is triggered. Because implanted Biomaterials elicit histaminic responses in the surrounding tissue, and histamine release is known to pro- mote rapid diapedesis of inf lammatory cells, we evaluated the possible role of histamine and mast cells in the recruitment of phagocytes to biomaterial implants. Using i.p. and s.c. im- plantation of polyethylene terephthalate disks in mice we find: (i) Extensive degranulation of mast cells, accompanied by histamine release, occurs adjacent to short-term i.p. implants. (ii) Simultaneous administration of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respec- tively) greatly diminishes recruitment and adhesion of both neutrophils (<20% of control) and monocytesymacrophages (<30% of control) to implants. (iii) Congenitally mast cell- deficient mice also exhibit markedly reduced accumulation of phagocytes on both i.p. and s.c implants. (iv) Finally, mast cell reconstitution of mast cell-deficient mice restores ''normal'' inf lammatory responses to biomaterial implants. We con- clude that mast cells and their granular products, especially histamine, are important in recruitment of inf lammatory cells to biomaterial implants. Improved knowledge of such re- sponses may permit purposeful modulation of both acute and chronic inf lammation affecting implanted Biomaterials.
John W. Eaton - One of the best experts on this subject based on the ideXlab platform.
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molecular basis of biomaterial mediated foreign body reactions
Blood, 2001Co-Authors: Wenjing Hu, Tatiana P Ugarova, John W. Eaton, Liping TangAbstract:Despite being inert and nontoxic, implanted Biomaterials often trigger adverse foreign body reactions such as inflammation, fibrosis, infection, and thrombosis. With regard to the inflammatory responses to biomaterial implants, it was previously found that a crucial precedent event was the spontaneous adsorption and denaturation of fibrinogen on implant surfaces. It was further found that interactions between the phagocyte integrin Mac-1 (CD11b/CD18) and one short sequence within the fibrinogen D domain (γ190-202; P1) at least partially explained phagocyte accumulation on implant surfaces. However, the reason that adsorbed fibrinogen is proinflammatory—while soluble fibrinogen clearly is not—remained obscure. In this study, therefore, the question of how fibrinogen is converted to a proinflammatory state when adsorbed to biomaterial surfaces is investigated. In soluble fibrinogen, the 13 amino acid P1 sequence was found to be hidden. However, the adsorption and denaturation of fibrinogen on the surfaces of commonly used Biomaterials lead to the exposure of P1 and a second neo-epitope, γ377-395 (P2), which also interacts with Mac-1 and is similarly occult in the soluble protein. The extent of biomaterial-mediated P1 and P2 exposure appears directly related to the severity of inflammatory responses to a test panel of Biomaterials. Finally, thrombin-mediated conversion of fibrinogen to fibrin also exposes both P1 and P2 epitopes. These observations may help explain both the inflammation caused by many types of implanted Biomaterials and that which occurs naturally following thrombotic events.
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mast cells mediate acute inflammatory responses to implanted Biomaterials
Proceedings of the National Academy of Sciences of the United States of America, 1998Co-Authors: Liping Tang, Timothy A Jennings, John W. EatonAbstract:Implanted Biomaterials trigger acute and chronic inflammatory responses. The mechanisms involved in such acute inflammatory responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, and adhesion to implant surfaces. We earlier observed that two chemokines-macrophage inflammatory protein 1alpha/monocyte chemoattractant protein 1-and the phagocyte integrin Mac-1 (CD11b/CD18)/surface fibrinogen interaction are, respectively, required for phagocyte chemotaxis and adherence to biomaterial surfaces. However, it is still not clear how the initial transmigration of phagocytes through the endothelial barrier into the area of the implant is triggered. Because implanted Biomaterials elicit histaminic responses in the surrounding tissue, and histamine release is known to promote rapid diapedesis of inflammatory cells, we evaluated the possible role of histamine and mast cells in the recruitment of phagocytes to biomaterial implants. Using i.p. and s. c. implantation of polyethylene terephthalate disks in mice we find: (i) Extensive degranulation of mast cells, accompanied by histamine release, occurs adjacent to short-term i.p. implants. (ii) Simultaneous administration of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respectively) greatly diminishes recruitment and adhesion of both neutrophils (<20% of control) and monocytes/macrophages (<30% of control) to implants. (iii) Congenitally mast cell-deficient mice also exhibit markedly reduced accumulation of phagocytes on both i.p. and s.c implants. (iv) Finally, mast cell reconstitution of mast cell-deficient mice restores "normal" inflammatory responses to biomaterial implants. We conclude that mast cells and their granular products, especially histamine, are important in recruitment of inflammatory cells to biomaterial implants. Improved knowledge of such responses may permit purposeful modulation of both acute and chronic inflammation affecting implanted Biomaterials.
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mast cells mediate acute inflammatory responses to implanted Biomaterials histamineyphagocytes
1998Co-Authors: Liping Tang, Imothy T A Jennings, John W. EatonAbstract:Implanted Biomaterials trigger acute and chronic inf lammatory responses. The mechanisms involved in such acute inf lammatory responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, and adhesion to implant surfaces. We earlier observed that two chemokines— macrophage inf lammatory protein 1aymonocyte chemoat- tractant protein 1—and the phagocyte integrin Mac-1 (CD11byCD18)ysurface fibrinogen interaction are, respec- tively, required for phagocyte chemotaxis and adherence to biomaterial surfaces. However, it is still not clear how the initial transmigration of phagocytes through the endothelial barrier into the area of the implant is triggered. Because implanted Biomaterials elicit histaminic responses in the surrounding tissue, and histamine release is known to pro- mote rapid diapedesis of inf lammatory cells, we evaluated the possible role of histamine and mast cells in the recruitment of phagocytes to biomaterial implants. Using i.p. and s.c. im- plantation of polyethylene terephthalate disks in mice we find: (i) Extensive degranulation of mast cells, accompanied by histamine release, occurs adjacent to short-term i.p. implants. (ii) Simultaneous administration of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respec- tively) greatly diminishes recruitment and adhesion of both neutrophils (<20% of control) and monocytesymacrophages (<30% of control) to implants. (iii) Congenitally mast cell- deficient mice also exhibit markedly reduced accumulation of phagocytes on both i.p. and s.c implants. (iv) Finally, mast cell reconstitution of mast cell-deficient mice restores ''normal'' inf lammatory responses to biomaterial implants. We con- clude that mast cells and their granular products, especially histamine, are important in recruitment of inf lammatory cells to biomaterial implants. Improved knowledge of such re- sponses may permit purposeful modulation of both acute and chronic inf lammation affecting implanted Biomaterials.
Brian Roderick Ward - One of the best experts on this subject based on the ideXlab platform.
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biophysical characterization of ovine forestomach extracellular matrix Biomaterials
Journal of Biomedical Materials Research Part B, 2011Co-Authors: Evan W Floden, S Malak, Melissa M Basiljones, Leonardo Negron, James N Fisher, Stan Lun, Sandi G Dempsey, Richard G Haverkamp, Brian Roderick Ward, Barnaby C H MayAbstract:Ovine forestomach matrix (OFM) is a native and functional decellularized extracellular matrix biomaterial that supports cell adhesion and proliferation and is remodeled during the course of tissue regeneration. Small angle X-ray scattering demonstrated that OFM retains a native collagen architecture (d spacing = 63.5 ± 0.2 nm, orientation index = 20°). The biophysical properties of OFM were further defined using ball-burst, uniaxial and suture retention testing, as well as a quantification of aqueous permeability. OFM biomaterial was relatively strong (yield stress = 10.15 ± 1.81 MPa) and elastic (modulus = 0.044 ± 0.009 GPa). Lamination was used to generate new OFM-based Biomaterials with a range of biophysical properties. The resultant multi-ply OFM Biomaterials had suitable biophysical characteristics for clinical applications where the grafted biomaterial is under load.
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biophysical characterization of ovine forestomach extracellular matrix Biomaterials
Journal of Biomedical Materials Research Part B, 2011Co-Authors: Evan W Floden, Melissa M Basiljones, Leonardo Negron, Sandi G Dempsey, Richard G Haverkamp, Sharif F Malak, J Fisher, Brian Roderick WardAbstract:Ovine forestomach matrix (OFM) is a native and functional decellularized extracellular matrix biomaterial that supports cell adhesion and proliferation and is remodeled during the course of tissue regeneration. Small angle X-ray scattering demonstrated that OFM retains a native collagen architecture (d spacing = 63.5 ± 0.2 nm, orientation index = 20°). The biophysical properties of OFM were further defined using ball-burst, uniaxial and suture retention testing, as well as a quantification of aqueous permeability. OFM biomaterial was relatively strong (yield stress = 10.15 ± 1.81 MPa) and elastic (modulus = 0.044 ± 0.009 GPa). Lamination was used to generate new OFM-based Biomaterials with a range of biophysical properties. The resultant multi-ply OFM Biomaterials had suitable biophysical characteristics for clinical applications where the grafted biomaterial is under load. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2011.
Evan W Floden - One of the best experts on this subject based on the ideXlab platform.
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biophysical characterization of ovine forestomach extracellular matrix Biomaterials
Journal of Biomedical Materials Research Part B, 2011Co-Authors: Evan W Floden, S Malak, Melissa M Basiljones, Leonardo Negron, James N Fisher, Stan Lun, Sandi G Dempsey, Richard G Haverkamp, Brian Roderick Ward, Barnaby C H MayAbstract:Ovine forestomach matrix (OFM) is a native and functional decellularized extracellular matrix biomaterial that supports cell adhesion and proliferation and is remodeled during the course of tissue regeneration. Small angle X-ray scattering demonstrated that OFM retains a native collagen architecture (d spacing = 63.5 ± 0.2 nm, orientation index = 20°). The biophysical properties of OFM were further defined using ball-burst, uniaxial and suture retention testing, as well as a quantification of aqueous permeability. OFM biomaterial was relatively strong (yield stress = 10.15 ± 1.81 MPa) and elastic (modulus = 0.044 ± 0.009 GPa). Lamination was used to generate new OFM-based Biomaterials with a range of biophysical properties. The resultant multi-ply OFM Biomaterials had suitable biophysical characteristics for clinical applications where the grafted biomaterial is under load.
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biophysical characterization of ovine forestomach extracellular matrix Biomaterials
Journal of Biomedical Materials Research Part B, 2011Co-Authors: Evan W Floden, Melissa M Basiljones, Leonardo Negron, Sandi G Dempsey, Richard G Haverkamp, Sharif F Malak, J Fisher, Brian Roderick WardAbstract:Ovine forestomach matrix (OFM) is a native and functional decellularized extracellular matrix biomaterial that supports cell adhesion and proliferation and is remodeled during the course of tissue regeneration. Small angle X-ray scattering demonstrated that OFM retains a native collagen architecture (d spacing = 63.5 ± 0.2 nm, orientation index = 20°). The biophysical properties of OFM were further defined using ball-burst, uniaxial and suture retention testing, as well as a quantification of aqueous permeability. OFM biomaterial was relatively strong (yield stress = 10.15 ± 1.81 MPa) and elastic (modulus = 0.044 ± 0.009 GPa). Lamination was used to generate new OFM-based Biomaterials with a range of biophysical properties. The resultant multi-ply OFM Biomaterials had suitable biophysical characteristics for clinical applications where the grafted biomaterial is under load. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2011.
Robert Klopfleisch - One of the best experts on this subject based on the ideXlab platform.
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The pathology of the foreign body reaction against Biomaterials.
Journal of Biomedical Materials Research Part A, 2016Co-Authors: Robert Klopfleisch, Friedrich JungAbstract:The healing process after implantation of Biomaterials involves the interaction of many contributing factors. Besides their in vivo functionality, Biomaterials also require characteristics that allow their integration into the designated tissue without eliciting an overshooting foreign body reaction (FBR). The targeted design of Biomaterials with these features, thus, needs understanding of the molecular mechanisms of the FBR. Much effort has been put into research on the interaction of engineered materials and the host tissue. This elucidated many aspects of the five FBR phases, that is protein adsorption, acute inflammation, chronic inflammation, foreign body giant cell formation, and fibrous capsule formation. However, in practice, it is still difficult to predict the response against a newly designed biomaterial purely based on the knowledge of its physical-chemical surface features. This insufficient knowledge leads to a high number of factors potentially influencing the FBR, which have to be analyzed in complex animal experiments including appropriate data-based sample sizes. This review is focused on the current knowledge on the general mechanisms of the FBR against Biomaterials and the influence of biomaterial surface topography and chemical and physical features on the quality and quantity of the reaction. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 927-940, 2017.
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macrophage reaction against Biomaterials in the mouse model phenotypes functions and markers
Acta Biomaterialia, 2016Co-Authors: Robert KlopfleischAbstract:Abstract The foreign body reaction (FBR) is a response of the host tissue against more or less degradation-resistant foreign macromolecular material. The reaction is divided into five different phases which involve most aspects of the innate and the adaptive immune system: protein adsorption, acute and chronic inflammation, foreign body giant cell formation and fibrosis. It is long known, that macrophages play a central role in all of these phases except for protein adsorption. Initially it was believed that the macrophage driven FBR has a complete negative effect on biocompatibility. Recent progress in biomaterial and macrophage research however describe macrophages as more than pure antigen phagocytosing and presenting cells and thus pro-inflammatory cells involved in biomaterial encapsulation and failure. Quite contrary, both, pro-inflammatory M1 macrophages, the diverse regulatory M2 macrophage subtypes and even foreign body giant cells (FBGC) are after necessary for integration of non-degradable Biomaterials and degradation and replacement of degradable Biomaterials. This review gives a comprehensive overview on the taxonomy of the currently known macrophage subtypes. Their diverging functions, metabolism and markers are summarized and the relevance of this more diverse macrophage picture for the design of Biomaterials is shortly discussed. Statement of Significance The view on role of macrophages in the foreign body reaction against Biomaterials is rapidly changing. Despite the initial idea that macrophage are mainly involved in undesired degradation and biomaterial rejection it becomes now clear that they are nevertheless necessary for proper integration of non-degradable Biomaterials and degradation of placeholder, degradable Biomaterials. As a pathologist I experienced a lack on a good summary on the current taxonomy, functions and phenotypes of macrophages in my recent projects on the biocompatibility of Biomaterials in the mouse model. The submitted review therefore intends to gives a comprehensive overview on the taxonomy of the currently known macrophage subtypes. Their diverging functions, metabolism and markers are summarized and the relevance of this more diverse macrophage picture for the design of Biomaterials is shortly discussed.