Background and activities
The strategy of my research group is to study the functions of the complement system, inflammasomes and Toll-like receptors in relation to signaling induced by microbes and cholesterol crystals. Our research points to new targets and strategies for treatment of inflammatory diseases. I am the director of Centre of Molecular Inflammation Research (CEMIR) which is a Centre of Excellence (https://www.ntnu.edu/cemir).
Scientific, academic and artistic work
A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database
- (2016) Dual inhibition of complement and Toll-like receptors as a novel approach to treat inflammatory diseases-C3 or C5 emerge together with CD14 as promising targets. Journal of Leukocyte Biology.
- (2016) Combined inhibition of complement and CD14 attenuates bacteria-induced inflammation in human whole blood more efficiently than antagonizing the toll-like receptor 4-MD2 complex. Journal of Infectious Diseases. vol. 214 (1).
- (2016) Effect of a single dose of the interleukin-6 receptor antagonist tocilizumab on inflammation and troponin T release in patients with non-ST-elevation myocardial infarction: a double-blind, randomized, placebo-controlled phase 2 trial. European Heart Journal. vol. 37 (30).
- (2016) Increased levels of legumain in plasma and plaques from patients with carotid atherosclerosis. Atherosclerosis.
- (2016) Cytokine profiles in human metapneumovirus infected children: Identification of genes involved in the antiviral response and pathogenesis. PLoS ONE. vol. 11:e0155484 (5).
- (2016) The intracellular C5 system is critical to DAMP sensing and cellular responses in human monocytes. Immunobiology.
- (2016) Complement activation by cholesterol crystals triggers a subsequent cytokine response. Molecular Immunology.
- (2016) Human endothelial cell activation by Escherichia coli and staphylococcus aureus is mediated by TNF and IL-1β secondarily to activation of C5 and CD14 in whole blood. Journal of Immunology. vol. 196 (5).
- (2016) Cholesterol crystals activate the lectin complement pathway via ficolin-2 and mannose-binding lectin: Implications for the progression of atherosclerosis. Journal of Immunology. vol. 196 (12).
- (2016) Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming. Science Translational Medicine. vol. 8 (333).
- (2016) Alginate microsphere compositions dictate different mechanisms of complement activation with consequences for cytokine release and leukocyte activation. Journal of Controlled Release. vol. 229.
- (2015) TLR8 senses Staphylococcus aureus RNA in human primary monocytes and macrophages and induces IFN-β production via a TAK1-IKKβ-IRF5 signaling pathway. Journal of Immunology. vol. 195 (3).
- (2015) The anti-inflammatory effect of combined complement and CD14 inhibition is preserved during escalating bacterial load. Clinical and Experimental Immunology. vol. 181 (3).
- (2015) The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis. Atherosclerosis. vol. 241 (2).
- (2015) CD14, TLR4 and TRAM Show Different Trafficking Dynamics During LPS Stimulation. Traffic : the International Journal of Intracellular Transport. vol. 16.
- (2015) CD14, TLR4 and TRAM Show Different Trafficking Dynamics During LPS Stimulation. Traffic : the International Journal of Intracellular Transport. vol. 16 (7).
- (2015) CD14 and complement crosstalk and largely mediate the transcriptional response to Escherichia coli in human whole blood as revealed by DNA microarray. PLoS ONE. vol. 10 (2).
- (2015) Gene expression profiling of Gram-negative bacteria-induced inflammation in human whole blood: The role of complement and CD14-mediated innate immune response. Genomics Data. vol. 5.
- (2015) A role for the adaptor proteins TRAM and TRIF in toll-like receptor 2 signaling. Journal of Biological Chemistry. vol. 290 (6).
- (2015) Reconstituted high-density lipoprotein attenuates cholesterol crystal-induced inflammatory responses by reducing complement activation. Journal of Immunology. vol. 195 (1).