Background
Globally, more than 300 million people have asthma. In Sweden, asthma prevalence is estimated at up to 10 %, pointing out that more than one million residents have current asthma, with one-third lacking adequate control of the disease. Severe asthma, estimated at around 3-5 %, is challenging to treat and is associated with significantly increased morbidity and mortality despite treatment representing a heavy burden for Swedish society with high societal costs, as asthma affects a younger population.
Severe asthma is a heterogeneous syndrome with several different phenotypes. To understand these phenotypes, we must define the dominant endotypes,i.e, the underlying inflammation.
Obese-related asthma represents a distinct severe asthma phenotype. Obese patients with asthma have more symptoms, more severe and frequent exacerbations, display reduced response to asthma medications, and subsequently, reduced quality of life. Underlying mechanisms include obesity´s effect on lung function mechanics and inflamed adipose tissue, inducing low-grade systemic inflammation.
The link between bacterial infections and asthma has gained interest recently, with many studies confirming the role of the microbiome in asthma development. Frequent infection leads to worsening asthma, with exacerbations and hospitalizations, and an increased risk for permanent airway structural changes, namely bronchiectasis.
Bronchiectasis is a chronic respiratory disease characterized by permanent bronchial dilatations and recurrent symptoms such as cough, expectoration, and respiratory infections. It is overrepresented in patients with severe asthma, with a prevalence of up to 25-40% compared to only 3% in a population of generally milder asthma, and it is associated with a higher risk of asthma-related hospitalizations.
Asthma and bronchiectasis are characterized by chronic inflammation orchestrating from T helper cells, such as Th1, Th2, and Th17.
Inflammation is protective as a response to invading microbes and noxious stimuli, i.e., allergens or tissue injury. However, without proper control, it leads to chronic inflammation, i.e., severe asthma and bronchiectasis. Thus, anti-inflammatory mechanisms such as the immunoregulatory T regulatory cells are also essential.
What we do
We perform clinical and translational studies on severe asthma and bronchiectasis using a bed-to-bench approach. Based on the clinical translation of the underlying inflammation, we aim to understand the regulation of chronic inflammation, with the ultimate purpose to identify new therapeutic targets.