Unit of Experimental Asthma and Allergy Research
Mechanisms and biomarkers in asthma
People with asthma suffer from repeated episodes of respiratory distress. This causes great suffering with anxiety, anxiety and impaired functioning in daily life. What triggers the asthma attacks is often allergic reactions, viral infections or air pollution. Asthmatic individuals react strongly to these reactions because they have hypersensitive airways. The cause of this airway hyperreactivity is hitherto unknown interactions between environment and heritage. This is further complicated by the fact that there are several asthma phenotypes.
The focus of our group is to define the mechanisms and molecules that cause airway contractions and hypersensitivity. The initial goal is that these investigations should lead to the help of asthmatics with special interventions with these problems. Using the acquired knowledge of the mechanisms that cause contractions and hypersensitivity in the airways, the next goal is to follow the signalling pathways upstream to find the reasons why this occurs.
To be able to carry out the research objectives, we use a translational research strategy. It includes an exchange of results from experiments at various levels such as in vivo and in vitro functional airway studies, study of tissue structures, secretion patterns, immunological and inflammatory processes, and expression of genes and proteins. For this, human tissue, animal experiments and isolated cells from both animal and human are used.
An important part of research is to define the different phenotypes of asthma. Over the past 15 years, a significant part of our work has been about how important lipid mediators are for the mechanisms of asthma. We have also shown that measuring them is a powerful tool for phenotyping in clinical studies of asthma. Through collaboration with national and international research groups, markers from different clinical cohorts (ENFUMOSA, BIOAIR, GA2LEN, U-BIOPRED, BIOCROSS and 3TR) are currently being investigated.