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Complement Activation Triggered by Biomaterial Surfaces: Mechanisms and Regulation
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
2003 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Today there are a vast number of medical devices in temporary or permanent contact with human tissues. Blood-biomaterial contact is known to trigger the complement system and results in generation of fluid phase anaphylatoxins C3a and C5a, and surface-bound C3b and iC3b. All these products together are able to attract and activate leukocytes and trigger release of inflammatory mediators leading to a systemic inflammation indirectly causing hemostatic problems and even organ failure. The aim of this study was to identify how complement is triggered on a biomaterial surface and to find ways to regulate this activation.

The finding that complement activation on biomaterials can be divided into initiation and amplification will facilitate regulation of complement activation biomaterial surfaces. This concept is also compatible with the two techniques to regulate complement activation on a surface.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis , 2003. , p. 45
Series
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1253
Keywords [en]
Immunology, Biomaterials, Biocompatibility, Blood, Complement
Keywords [sv]
Immunologi
National Category
Immunology in the medical area
Research subject
Clinical Immunology
Identifiers
URN: urn:nbn:se:uu:diva-3410ISBN: 91-554-5610-3 (print)OAI: oai:DiVA.org:uu-3410DiVA, id: diva2:162710
Public defence
2003-05-20, Rudbeckssalen, Rudbeck Laboratory, Uppsala, 09:15
Opponent
Supervisors
Available from: 2003-04-24 Created: 2003-04-24 Last updated: 2018-01-13Bibliographically approved
List of papers
1. Complement activation on a model biomaterial surface: Binding of C3b via the alternative pathway amplification loop to plasma proteins adsorbed to the surface
Open this publication in new window or tab >>Complement activation on a model biomaterial surface: Binding of C3b via the alternative pathway amplification loop to plasma proteins adsorbed to the surface
Manuscript (Other academic)
Identifiers
urn:nbn:se:uu:diva-90375 (URN)
Available from: 2003-04-24 Created: 2003-04-24 Last updated: 2010-01-13Bibliographically approved
2. C3 Adsorbed to a Polymer Surface Can Form an Initiating Alternative Pathway Convertase
Open this publication in new window or tab >>C3 Adsorbed to a Polymer Surface Can Form an Initiating Alternative Pathway Convertase
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2002 In: Journal of Immunology, ISSN 0022-1767, Vol. 168, no 11, p. 5786-5791Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-90376 (URN)
Available from: 2003-04-24 Created: 2003-04-24Bibliographically approved
3. Binding of a model regulator of complement activation (RCA) to a biomaterial surface: surface-bound factor H inhibits complement activation
Open this publication in new window or tab >>Binding of a model regulator of complement activation (RCA) to a biomaterial surface: surface-bound factor H inhibits complement activation
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2001 In: Biomaterials, ISSN 0142-9612, Vol. 22, no 17, p. 2435-2443Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-90377 (URN)
Available from: 2003-04-24 Created: 2003-04-24Bibliographically approved
4. Optimal heparin surface concentration and antithrombin binding capacity as evaluated with human non-anticoagulated blood in vitro
Open this publication in new window or tab >>Optimal heparin surface concentration and antithrombin binding capacity as evaluated with human non-anticoagulated blood in vitro
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2003 (English)In: Journal of Biomedical Materials Research, ISSN 0021-9304, E-ISSN 1097-4636, Vol. 67, no 2, p. 458-466Article in journal (Refereed) Published
Abstract [en]

Contact between blood and a biomaterial surface takes place in many applications and is known to activate the coagulation and complement systems. Heparin surface coatings have been shown to reduce blood activation upon contact with artificial surfaces. To establish the optimal heparin surface concentration, blood was incubated in a tubing loop model at 37 degrees C. The tubing was coated with different surface concentrations of heparin and rotated at three different velocities. We demonstrate that the blood compatibility of a surface with regard to coagulation, complement, and platelet activation can be improved by increasing the heparin surface concentration in the 6-12 pmol antithrombin/cm2 concentration interval. The binding of factor H is not influenced by the increased heparin surface concentration, suggesting that this factor is not the primary regulator of complement on heparin surfaces. In addition, the heparin coating has no effect on the complement activation that occurs on gas surfaces in extracorporeal circuits.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-90378 (URN)10.1002/jbm.a.10104 (DOI)14566786 (PubMedID)
Available from: 2003-04-24 Created: 2003-04-24 Last updated: 2017-12-14Bibliographically approved

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