Pathologic changes of the airway cause asthma.
This theory was first formulated by Huber & Kössler in their first study investigating the structural pathologies of the asthmatic lung in 1922. The asthmatic airway is characterised by two pathologies:
- chronic inflammation and
- thickening of the airway wall results from increased volume of tissue.
This reduces the airway lumen and thereby hinders breathing. In addition, the increased muscles constrict more during an asthma attack and further reduce the airway lumen, leading to the feeling of “suffocation”.
The inflammation can be well reduced by the available medication, but none of them has any effect on the airway wall changes. This mainly excludes inflammation as the cause of the structural changes in the airway wall. New studies in humans also rejected the concept that the structural changes in the airway wall develop slowly over several years, as it has been shown that the permanent changes can occur as fast as within 4 days.
Together with our colleagues from Sydney (Australia – the country with the highest asthma incidence in the world), Manitoba (Canada), Groningen (Holland) and Xi’an (China), we are searching for the cause of the structural changes in the asthmatic airways. Since animal models did not help to understand the human disease, we exclusively work with human tissue and cells generated from this tissue. Our studies yielded interesting new results which can explain how different asthma triggers (pollen, dust, smoke, hair etc.) induce the same tissue changes in the asthmatic airways. This new knowledge has changed our view of the initiation of asthma. The next step is to find a therapy and medicaments which could interrupt or reverse this mechanism. In order to turn this new knowledge into new therapies, we need more time and funding to develop novel therapeutic strategies. For that, we need your help and support. The cost of our research be about 200,000 CHF annually and are funded in part by the Swiss National Science Foundation and research contracts.
Recent achievements: Together with our colleagues from Xi’an, China, we described a new pathology which causes remodelling of the asthmatic airways (Sun Q et al. JACI 2016). Importantly, the constitutive activity of a mitochondria regulating protein (PRMT1) may present the merging event of several asthma and cell type specific pathologies that were described by us and others earlier. Future studies will focus on the cause of the constitutive activation of PRMT1 and medications which can normalise it.