The University of Oslo is closed and the public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
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Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Associate Professor Reinhard Würzner, Innsbruck Medical University, Austria
- Second opponent: Associate Professor Leendert A. Trouw, Leiden University Medical Center, The Netherlands
- Third member and chair of the evaluation committee: Associate Professor Carola Henriksen, University of Oslo
Chair of the Defence
Professor Emeritus Jarle Vaage, University of Oslo
Principal Supervisor
Researcher Per H. Nilsson, University of Oslo
Summary
Inflammation is a biological response of the body to danger. The first line of host defences is by the innate immune system. The innate response is initiated by recognition of danger either through patterns on the surface of microorganisms or on damaged cells by complement proteins (paper I). After initiation, sequential enzymatic reactions release activation fragments inducing inflammation in order to achieve homeostasis. Concurrent complement crosstalk with other systems such as the coagulation cascade can influence the outcome of inflammation (paper II) through activation of cellular response signalling (paper III), contact activation and thrombosis. Production of inflammatory indicators can be reliant on other cell types (paper IV) where here the focus is to study platelet influence on monocytes.
The overall aim presented in this thesis was to investigate mechanisms for complement activation and describe how complement activation triggers an inflammatory response in a human whole blood or plasma environment. Recognition properties, crosstalk with the coagulation cascade and platelets, as well as, an overall characterisation of the thromboinflammatory response to bacteria were studied through the development of new methodology. We found that complement activation is not reliant upon properdin recognition for certain targets and rather necessitated C3b deposition. In whole blood, thrombin did not cleave C5 unless plasma was acidified or purified components were supplemented to C5-deficient serum. However, thrombin could modulate the inflammatory response when co-incubated with bacteria as demonstrated by cytokine production even without direct thrombin activation to complement. Interleukin (IL)-8 production was particularly susceptible to regulation by thrombin influences.
Additional information
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