What we do
It is recognized that around 10% of the global population is affected by chronic obstructive pulmonary disease (COPD), an inflammatory airway disorder that accounts for more than three million deaths each year. What is less recognized is that the mortality in very severe COPD is comparable to that of lung cancer. The cost for the entire patient group with COPD is estimated to exceed 3% of the total health care budget in the European union.
The main risk factor for contracting COPD is long-term exposure to tobacco smoke but it is believed that other exposures account for a substantial portion of cases at the global level. Examples of other exposures include air pollution from burning of biomass other that tobacco, particles in traffic environment and certain types of dust in the building industry. Events early in life, such as premature birth, pneumonia and severe asthma, also constitute known risk factors. In patients with COPD, repeated airway infections constitute a risk factor for disease progression, especially when the is concomitant chronic phlegm (chronic bronchitis) and bronchiectasis, a disorder with impaired mucociliary transport in the airways.
It is known that patients with COPD have very variable prognosis, and current diagnostic methods are not sufficient to identify individual patients at risk for poor prognosis. Current diagnostic methods are not sufficient to predict the therapeutic responsiveness for the individual patient either. These problems constitute a major practical obstacle for health care. Additionally, there is currently a lack of efficient therapy for the specific inflammatory profile that is most common, and that is linked to the increased susceptibility for infections in patients with COPD. All these problems relate to a general lack of understanding of fundamental disease mechanisms at the cellular and molecular level.
The fact that there is an increased susceptibility to infections in COPD despite the local accumulation of antimicrobial immune cells in the airways represents something of a paradox. Since several years back, our research group conducts research based upon the hypothesis that certain exposure causes fundamental alteration in host defence, especially the critical cytokine signalling that controls local accumulation and activation of immune cells for killing of microbes. For the purpose of identifying critical alterations in antimicrobial host defence, we characterize quantitative alterations in relevant cytokines in the airways of smokers with and without COPD and compare them with the corresponding cytokine signalling in healthy and non-smoking controls. We also characterize bacterial microbiota in relation to cytokine signalling. To evaluate which immune cells and cytokines are most relevant, we also investigate healthy subjects with and without microbial stimulation in the airways, as well as patients with pneumonia. To delineate specific cellular and molecular mechanisms, we use human cell models ex vivo. By combining these different studies, we can identify new cellular and molecular targets for diagnosis, monitoring and therapy of COPD and its comorbidities, ultimately for prevention as well.