Kolbjørn Högåsen

Innlandet Hospital Trust

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Tom Eirik Mollnes

Oslo University Hospital

M Harboe

University of Oslo

Torstein Hovig

Oslo University Hospital

Vibeke Videm

Norwegian University of Science and Technology

Erik Fosse

University of Oslo

Arnt E. Fiane

University of Oslo

O. J. Mellbye

University of Oslo

J. H. Jansen

Norwegian University of Life Sciences

Peter Garred

Rigshospitalet

Tom E. Mollnes

Oslo University Hospital

Cooperative Institutions

University of Oslo

Oslo University Hospital

Nordland Hospital

Norwegian University of Science and Technology

UiT The Arctic University of Norway

Institutt for Eksperimentell Medisinsk Forskning

University College London

Ludwig Boltzmann Institute for Experimental and Clinical Traumatology

Institute of Immunology

Norwegian Institute of Public Health

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Centrifugal pump and heparin coating improves cardiopulmonary bypass biocompatibility

The Annals of Thoracic Surgery (1996)

Oddvar Moen Erik Fosse Einar Dregelid Vibeke Brockmeier Conny Andersson

Activated clotting time

Extracorporeal circulation

10.1016/0003-4975(96)00492-4

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Citations (96)

Low Prevalence of Complement Deficiencies among Patients with Meningococcal Disease in Norway

Scandinavian Journal of Immunology (1993)

Kolbjørn Högåsen Terje E. Michaelsen O. J. Mellbye G Bjune

Sera from 98 individuals who had survived meningococcal disease were analysed for classical and alternative pathway haemolytic activity and the complement components C3. C4 and properdin. No complete deficiency was found. However, median properdin concentration was only 86% in the disease group compared with the controls (P<0.001). Properdin was also significantly lower in serogroup C disease (median 76%.) compared with serogroup B disease (median 90%, P = 0.005). Severe properdin deficiency is an established risk factor for meningococcal disease. The present data may indicate that even moderately reduced properdin level can increase the risk of developing meningococcal disease.

Properdin

Complement factor B

10.1111/j.1365-3083.1993.tb03323.x

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Citations (21)

Both Plasma- and Leukocyte-Associated C5a Are Essential for Assessment of C5a Generation In Vivo

The Annals of Thoracic Surgery (1997)

Geir Hetland Oddvar Moen Kåre Bergh Kolbjørn Högåsen C. Erik Hack

10.1016/s0003-4975(96)01255-6

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Citations (16)

Effect of filtration and storage of platelet concentrates on the production of the chemotaxins C5a, interleukin 8, tumor necrosis factor alpha, and leukotriene B₄

Transfusion (1998)

Geir Hetland Tom E. Mollnes Kerstin Bergh Kolbjørn Högåsen U. E. Bergerud

BACKGROUND: The production in platelet concentrates (PCs) of C3 activation products (C3bc), terminal complement complex (TCC), and chemotaxins C5a, interleukin (IL)‐8, tumor necrosis factor alpha (TNFalpha), and leukotriene B4 (LTB4) and the proposed reduction in concentration of the chemotaxins by white cell reduction were examined. STUDY DESIGN AND METHODS: Samples were collected from supernatants of PCs produced by apheresis (apheresis PCs) or from buffy coats (BC PCs) immediately after the production, after white cell‐reduction filtration on Day 1, and after 5‐day storage, and examined by enzyme immunoassays. RESULTS: Complement was activated in all PCs during storage, and the concentration of activation products was not influenced by prestorage filtration. In prestorage white cell‐reduced BC PCs, only C3bc levels increased. Levels of IL‐8, TNFalpha, and LTB4 increased during storage of apheresis PCs, but not in filtered units, except for LTB4. In contrast, levels of IL‐8 decreased after storage of filtered BC PCs. C5a correlated significantly with IL‐8, which also correlated with TNFalpha and LTB4. CONCLUSION: Both C5a and TNFalpha generation in apheresis PCs seem to induce white cell IL‐8 production, which mediates cellular LTB4 release. Prestorage white cell reduction is recommended for reducing chemotactic cytokine and leukotriene levels in all PCs. Production of BC PCs is recommended to achieve less complement activation, which is not affected by filtration.

Leukotriene B4

10.1046/j.1537-2995.1998.38198141493.x

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Citations (23)

En 52 år gammel kvinne med feber og lungesvikt

Tidsskrift for Den norske legeforening (2009)

Ingrid Ødegård Kolbjørn Högåsen Dag Paulsen Helge Scott

10.4045/tidsskr.09.0167

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Citations (1)

Attenuation of Changes in Leukocyte Surface Markers and Complement Activation With Heparin-Coated Cardiopulmonary Bypass

The Annals of Thoracic Surgery (1997)

Oddvar Moen Kolbjørn Högåsen Erik Fosse Einar Dregelid Vibeke Brockmeier

P-selectin

Activated clotting time

10.1016/s0003-4975(96)00743-6

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Citations (128)

Acquired C3 deficiency in patients with alcoholic cirrhosis predisposes to infection and increased mortality.

Gut (1997)

Christian Homann Kim Varming Kolbjørn Högåsen Tom E. Mollnes Niels Graudal

BACKGROUND: Acquired deficiencies of certain complement proteins and impaired opsonisation activity have been implicated in the pathogenesis of the increased susceptibility to infections of patients with alcoholic cirrhosis. METHODS: Serum concentrations of C3 and C4, plasma concentrations of C3bc, C9, and the terminal C5b-9 complement complex (TCC), and haemolytic complement activity (classic and alternative pathway) of serum, and serum opsonic activity were determined in 46 patients with compensated alcoholic cirrhosis, 31 who were decompensated, and in 15 healthy subjects. After 19 months (median) the investigated variables were analysed for their use in prognosis of recurrent infections and survival. RESULTS: C3 and C4 concentrations and the haemolytic complement activity of the alternative pathway were decreased in decompensated cirrhotic patients compared with controls (p < 0.01). Univariate analysis (log rank test) showed that low concentrations (< or = lower quartile) of C3 (p < 0.001) and C3bc (p < 0.05), haemolytic complement activity of the alternative pathway (p < 0.01) and classic pathway (p < 0.05), and decompensated cirrhosis (p < 0.001) were associated with an increased risk of infection and increased mortality. Multivariate (Cox) analysis showed that low C3 concentrations and decompensation of cirrhosis were significant predictors of infections and mortality (p < 0.02). CONCLUSIONS: Low serum C3 concentrations and decreased haemolytic complement function predisposes to infection and increased mortality in patients with alcoholic cirrhosis.

Properdin

Decompensation

Pathogenesis

Univariate analysis

10.1136/gut.40.4.544

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Citations (127)

Effects on complement activation and cytokine (TNF‐α and IL‐8) release of infusion of anti‐TNF‐antibodies or a xanthine derivative (HWA 138) in septic baboons

Acta Anaesthesiologica Scandinavica (1996)

Anders Bengtsson Heinz Redl G. Schlag Tom Eirik Mollnes Kolbjørn Högåsen

Background. Sepsis and septic shock lead to activation of the complement cascade and to the release of pro‐inflammatory cytokines. Methods. The effects of E coli infusion and of infusion of anti‐TNF antibodies and a xanthine derivative (HWA 138) on complement activation and cytokine release was evaluated in 17 baboons. All animals received 5×10 8 live bacteria per kg body weight. Five animals received only bacteria, five received in addition 0.5 mg per kg body weight of anti‐TNF‐antibody, and seven received an infusion of 6 mg per kg body weight of HWA 138 in addition to the bacteria. Results. In baboons receiving 5×10 8 live E coli per kg body weight increased plasma levels of TCC, TNF‐α and IL‐8 were found. The release of TNF‐α was lower in the group receiving HWA 138 at 2 h after the infusion. In baboons receiving an infusion of anti‐TNF antibody the concentration of IL‐8 was lower at 2 and 4 h than in animals receiving just E coli or HWA 138. Conclusion. Infusion of anti‐TNF‐antibody before E coli infusion will decrease the formation of IL‐8. Infusion of HWA 138 before the E coli infusion will also inhibit the formation of TNF‐α.

10.1111/j.1399-6576.1996.tb04427.x

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Citations (11)

A New Model for Evaluation of Biocompatibility: Combined Determination of Neoepitopes in Blood and on Artificial Surfaces Demonstrates Reduced Complement Activation by Immobilization of Heparin

Artificial Organs (1995)

Tom Eirik Mollnes Johan Riesenfeld Peter Garred Eva Nordström Kolbjørn Högåsen

Abstract: An in vitro technique was developed for assessment of the biocompatibility of materials for use in clinical applications. Artificial materials were exposed to blood, and the resulting complement activation was quantified both in the plasma and on the material surface by enzyme immunoassays based on monoclonal antibodies specific for neoepitopes exposed in complement activation products. Several materials were evaluated, and the effect of surface modifications, including end–point immobilized heparin, was studied. The results revealed widely varying complement activation properties of the different materials and confirmed that heparin markedly improves biocompatibility. The present method is superior to analysis limited to either the fluid phase or solid phase since certain materials adsorb activation products (exemplified by Tecoflex) whereas others do not although activation was evident from fluid–phase assay (silicone). Furthermore, direct determination of activation–specific neoepitopes on the surface represents an improvement compared with previously described methods for detection of adsorbed components.

Biocompatibility

10.1111/j.1525-1594.1995.tb02450.x

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Citations (59)

Low levels of vitronectin and clusterin in acute meningococcal disease are closely associated with formation of the terminal-complement complex and the vitronectin-thrombin-antithrombin complex

Infection and Immunity (1994)

Kolbjørn Högåsen Tom Eirik Mollnes P Brandtzæg

Patients with terminal complement deficiencies and thus impaired lytic efficiency have a highly increased likelihood of contracting invasive meningococcal infections but generally experience a mild disease course. Deficiencies of lysis inhibitors might therefore be associated with severe disease. We have quantified the complement lysis inhibitors vitronectin and clusterin, as well as complexes containing the proteins, in plasma from patients with acute meningococcal disease. At hospital admission, the median vitronectin concentrations were 0.10 (range, 0.04 to 0.17) g/liter in 10 septic patients and 0.19 (0.09 to 0.47) g/liter in 14 nonseptic patients (P = 0.001). The corresponding clusterin concentrations were 0.09 (0.01 to 0.13) and 0.14 (0.06 to 0.29) g/liter (P = 0.005). The vitronectin-thrombin-antithrombin complex concentration was 1.8 (0.22 to 35.6) arbitrary units (AU)/ml in septic patients, but the complex was not detectable in most nonseptic patients (< 0.10 to 0.16 AU/ml) (P < 0.0001). The corresponding levels of the terminal complement complex (contains vitronectin and clusterin) were 4.4 (3.6 to 20.1) and 2.6 (1.6 to 4.7) AU/ml (P = 0.0005). We found no evidence of constitutively low levels of vitronectin or clusterin in patients contracting meningococcal disease. The low levels of the proteins may partly be explained by hemodilution, extravasation, and increased consumption due to incorporation into complexes which are quickly removed from circulation.

Clusterin

Anaphylatoxin

10.1128/iai.62.11.4874-4880.1994

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Citations (28)