Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with a median survival of 3 years. Although new medications with some beneficial effect for stable IPF disease have been developed, their exact working mechanisms are still unknown.
We are interested in dissecting and understanding the pathways which are involved in these anti-fibrotic treatments in order to improve the efficiency of medications and ultimately the prognosis of the patients.
Further, the disease course of IPF patients is variable and so-called acute exacerbations lead to a considerable loss of lung function without recovery or directly result in death. The etiology and the role of exacerbation in IPF are unknown. More knowledge about cellular and molecular mechanisms is urgently needed to establish new diagnostic tools and treatment strategies.
We are investigating the role of Toll like receptor 4 (TLR4) and its regulatory mediators in IPF pathogenesis. We are also interested in individual responses of current drug treatments for IPF as a new and personalized approach for this disease.
In order to dissect which pathways are involved and react differently in IPF, we mainly use in vitro cellular systems with primary human cells. Pro-fibrotic gene responses of primary human fibroblasts are analyzed by different tools (RT-qPCR, ELISA, immunofluorescence, immunohistochemistry, Western blot etc.). We also address translational questions with human samples from clinical research projects at the Inselspital of Bern to discover new biomarkers.
It is a major goal of our group to investigate clinical challenges with basic science tools and translate basic research findings into useful practical applications in clinics.