Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Associate Professor Thomas Truelsen, University of Copenhagen
- Second opponent: Professor Knut Tore Lappegård, UiT - The Arctic University of Norway
- Third member and chair of the evaluation committee: Professor Angelika Sorteberg, University of Oslo
Chair of the Defence
Professor II Mona Kristiansen Beyer, University of Oslo
Principal Supervisor
Professor Mona Elisabeth Skjelland, University of Oslo
Summary
This thesis investigated the role of the human microbiota and its metabolites in advanced carotid atherosclerosis, a major contributor to ischemic stroke. The study explored how microbial composition, function, and host–microbe interactions influence plaque vulnerability. Using a cross-sectional design, patients with moderate and severe carotid stenosis were compared to healthy controls through analyses of fecal, oral, blood, and plaque samples.
Findings showed that patients with advanced atherosclerosis had increased fecal butyric acid levels, likely reflecting both enhanced microbial production and impaired intestinal absorption, alongside markers of gut barrier dysfunction and immune activation. Oral microbiota analysis revealed reduced intra-individual diversity and distinct inter-individual diversity in patients compared to controls. In addition, symptomatic patients (i.e. TIA or ischemic stroke within three months) had an increased abundance of Eikenella compared to asymptomatic patients. Bacterial DNA from common oral pathogens were detected in carotid plaques, suggesting microbial translocation. Additionally, patients exhibited lower circulating levels of indole-3-propionic acid, a metabolite linked to anti-inflammatory effects, which correlated with systemic inflammation.
Taken together, the results support a model in which gut dysbiosis, impaired barrier integrity, and oral bacterial translocation contribute to inflammation and plaque instability, highlighting the microbiota as a potential target for improved risk assessment and therapeutic strategies.
Additional information
Contact the research support staff.