The awareness of chronic inflammatory lung diseases (CILD) and how they affect a patient’s life, as well as their social surrounding and families, is low, while the prevalence of asthma and chronic obstructive pulmonary disease (COPD) is continuously increasing worldwide. In 2016, the European Union has estimated that around 50% of chronic inflammatory diseases are misdiagnosed and inadequately treated in Europe. Therefore, it is surprising how little attention is given to the impact of CILD by society.
Now, leading experts based at the University Hospital Basel have begun to re-investigate the pathogenesis of CILD. In order to find a cure or better therapy, it is necessary to understand the origin of the diseases. Only then will it be possible to develop new disease-specific diagnostic tools and personalised therapies.
This booklet looks specifically into:
- Genetic or epigenetic pre-disposition for CILD;
- The possible role of microRNAs in the cause of CILD; and
- The epithelial-mesenchymal-trophic-unit (EMTU) function and CILD.
According to the World Health Organization (WHO), 280 million people suffer from asthma during their life and approximately 40% of all children suffer from asthma like symptoms during childhood, and in some cases the disease becomes a lifelong burden.
The initiating event(s) leading to the pathogenesis of asthma is not well understood and the long-held hypothesis that chronic inflammation of the airway is the major cause of all other asthma pathologies has been challenged in recent years.
Today, airway wall remodelling is regarded as a pathology that is independent of inflammation and may even cause inflammation. However, none of these ideas can be proven or rejected. The current available medications allow symptom control but do not provide a cure. There is only one therapy which seems to lastingly reduce airway wall remodelling in severe asthma: bronchial thermoplasty.
Chronic obstructive pulmonary disease (COPD)
Different to asthma, COPD is characterised by constantly declining lung function, chronic inflammation and increased lung tissue remodelling. In late stage COPD, the lung’s structure declines and tissue structures disappear, finally leading to death.
In Europe and the Americas, cigarette smoking was assumed to be the major cause of COPD, while only 2% of patients develop COPD due to a genetic disorder (alpha1-antitrypsin deficiency). In less developed countries, cooking and heating with open fires was regarded as the major cause for COPD, often combined with cigarette smoking.
When looking into COPD patients, experts noted a cause of the disease as an imbalance of tissue building and degrading enzymes.
However, the mechanism behind this de-regulated tissue turn-over remains unknown.