About this project
IBD is characterised by increased migration of neutrophils to the inflamed intestine. Elevated levels of faecal-calprotectin indicate neutrophil and monocyte activity and the marker seems to correlate with endoscopic disease activity and histological findings. Increased levels of the faecal marker eosinophil protein X (EPX) and eosinophil cationic protein (ECP), reflecting eosinophil activity, have also been observed in IBD. At present we are exploring the role of fecal markers, neutrophils and eosinophils in the development of IBD in collaboration with Associate Professor Marie Carlsson, Uppsala University. Small molecules like defensins seems to play an important role in IBD and we are now launching a project where we will address to which extent the observed dysregulation is a secondary phenomenon or a primary defect in the pathogenesis of the disease.
The adaptive immune response also plays an important role in IBD. To evaluate T cell ontogeny in human IBD, so-called TcR-rearrangement excision circles (TRECs) can be analyzed. Previous data suggest that recent thymic emigrants are recruited rapidly to the inflamed mucosa. We are now together with Professor Elisabeth Hultgren Hörnqvist trying to explore the role of genetic predisposition in a twin model with respect to these findings.