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Complement Activation Triggered by Biomaterial Surfaces: Mechanisms and Regulation
Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
2003 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
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.

sted, utgiver, år, opplag, sider
Uppsala: Acta Universitatis Upsaliensis , 2003. , s. 45
Serie
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1253
Emneord [en]
Immunology, Biomaterials, Biocompatibility, Blood, Complement
Emneord [sv]
Immunologi
HSV kategori
Forskningsprogram
klinisk immunologi
Identifikatorer
URN: urn:nbn:se:uu:diva-3410ISBN: 91-554-5610-3 (tryckt)OAI: oai:DiVA.org:uu-3410DiVA, id: diva2:162710
Disputas
2003-05-20, Rudbeckssalen, Rudbeck Laboratory, Uppsala, 09:15
Opponent
Veileder
Tilgjengelig fra: 2003-04-24 Laget: 2003-04-24 Sist oppdatert: 2022-03-11bibliografisk kontrollert
Delarbeid
1. Complement activation on a model biomaterial surface: Binding of C3b via the alternative pathway amplification loop to plasma proteins adsorbed to the surface
Åpne denne publikasjonen i ny fane eller vindu >>Complement activation on a model biomaterial surface: Binding of C3b via the alternative pathway amplification loop to plasma proteins adsorbed to the surface
Manuskript (Annet vitenskapelig)
Identifikatorer
urn:nbn:se:uu:diva-90375 (URN)
Tilgjengelig fra: 2003-04-24 Laget: 2003-04-24 Sist oppdatert: 2010-01-13bibliografisk kontrollert
2. C3 Adsorbed to a Polymer Surface Can Form an Initiating Alternative Pathway Convertase
Åpne denne publikasjonen i ny fane eller vindu >>C3 Adsorbed to a Polymer Surface Can Form an Initiating Alternative Pathway Convertase
Vise andre…
2002 Inngår i: Journal of Immunology, ISSN 0022-1767, Vol. 168, nr 11, s. 5786-5791Artikkel i tidsskrift (Fagfellevurdert) Published
Identifikatorer
urn:nbn:se:uu:diva-90376 (URN)
Tilgjengelig fra: 2003-04-24 Laget: 2003-04-24bibliografisk kontrollert
3. Binding of a model regulator of complement activation (RCA) to a biomaterial surface: surface-bound factor H inhibits complement activation
Åpne denne publikasjonen i ny fane eller vindu >>Binding of a model regulator of complement activation (RCA) to a biomaterial surface: surface-bound factor H inhibits complement activation
Vise andre…
2001 Inngår i: Biomaterials, ISSN 0142-9612, Vol. 22, nr 17, s. 2435-2443Artikkel i tidsskrift (Fagfellevurdert) Published
Identifikatorer
urn:nbn:se:uu:diva-90377 (URN)
Tilgjengelig fra: 2003-04-24 Laget: 2003-04-24bibliografisk kontrollert
4. Optimal heparin surface concentration and antithrombin binding capacity as evaluated with human non-anticoagulated blood in vitro
Åpne denne publikasjonen i ny fane eller vindu >>Optimal heparin surface concentration and antithrombin binding capacity as evaluated with human non-anticoagulated blood in vitro
Vise andre…
2003 (engelsk)Inngår i: Journal of Biomedical Materials Research, ISSN 0021-9304, E-ISSN 1097-4636, Vol. 67, nr 2, s. 458-466Artikkel i tidsskrift (Fagfellevurdert) 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.

HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-90378 (URN)10.1002/jbm.a.10104 (DOI)14566786 (PubMedID)
Tilgjengelig fra: 2003-04-24 Laget: 2003-04-24 Sist oppdatert: 2017-12-14bibliografisk kontrollert

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