Taman disputerer for ph.d.-graden i helsevitenskap og vil offentlig forsvare avhandlingen: “Epigenetics in Inflammatory Bowel Disease Contribution of DNA methylation to Ulcerative Colitis pathogenesis”
Prøveforelesning starter kl. 10.15
Prøveforelesning har følgene tittel: «The role of gut microbiota and genetics in rheumatological systemic diseases”
Disputas starter kl 12.00
Auditoriet er åpent for publikum, men vil også bli strømmet. Opptak av disputasen vil være tilgjengelig i et døgn.
The auditorium is open to the public, but it will also be streamed. A recording of the disputation will be available for 24 hours.
Populærvitenskapelig sammendrag av avhandlingen:
Inflammatory bowel disease (IBD) affects approximately 6.8 million people worldwide, and more than 1.3 million people in Europe alone. Patients affected with IBD have a significantly reduced quality of life. IBD is a recurring chronic inflammatory disease of the gastrointestinal tract. It consists of two subtypes, Crohn’s disease (CD) and ulcerative colitis (UC). IBD can have a devastating consequence for those affected. IBD is difficult to diagnose, and symptoms include abdominal pain, rectal bleeding, and diarrhea. Patients can suffer for years before they are diagnosed and treated. Unfortunately, the causes and mechanisms behind IBD is still not fully understood. Genetics plays a role in disease development; however, it cannot explain the recent increase in disease prevalence. IBD is likely a result of the interplay between genetics, environmental factors, microbiome, and nutrition.
Epigenetics, the interaction between genetics and environmental factors has been highlighted as another important factor in IBD. Epigenetics can temporarily or permanently change gene expression without changing the DNA sequence itself. Epigenetic regulation occurs through different mechanisms, the most studied of these mechanisms is DNA methylation. In our research we wanted to investigate how DNA methylation contributes to UC development.
Next generation sequencing (NGS) technology was used to sequence both DNA and RNA from untreated UC patients and healthy individuals. Comparing UC with healthy controls revealed that DNA methylation differs in disease severity and gender.
In mild UC patients, we found that methylation occurred to a greater extent (hypermethylation) in genes that reduce inflammation thus helping keep the body in balance. In contrast, genes involved in the immune response were less methylated (hypomethylation). Interestingly, in severe UC patients’ genes involved in anti-inflammatory response were hypomethylated, and therefore they can reduce the inflammation degree.
Professor Ruth Hracky Paulssen, Institutt for klinisk medisin, Det helsevitenskapelige fakultet, UiT Norges arktiske universitet
Professor emeritus Jon Ragnar Florholmen, Institutt for klinisk medisin, Det helsevitenskapelige fakultet, UiT Norges arktiske universitet
Førsteamanuensis Jan Marsal, Skåne University Hospital, Lund – 1. opponent
Senior Scientist PhD Robert Lyle, Oslo University Hospital – 2. Opponent
Førsteamanuensis Jorunn Pauline Cavanagh, IKM Det helsevitenskapelige fakultet, UiT Norges arktiske universitet – leder av komité.
Professor Sigrid Brækkan, Institutt for klinisk medisin, Det helsevitenskapelige fakultet, UiT Norges arktiske universitet