Asthma is a heterogeneous airway disease with multiple phenotypes. Severe asthma is in only a minority of patients, but this patient cohort present relevant comorbidities and represent a large socioeconomic burden. Bronchiectasis is one of the most frequent comorbidities in severe asthma, characterized by pathological dilation of the airways. The presence of bronchiectasis may mimic asthma symptoms, resulting in poor asthma control with persistent clinical symptoms and difficult disease management. The mechanisms through which asthma promotes the evolution and development of bronchiectasis remain obscure. Moreover, it is uncertain whether a cause-effect relationship exists between asthma and bronchiectasis, but there is no doubt that asthma and bronchiectasis share some common features with respect to the innate immune activation and airway remodelling. Although in bronchiectasis the role of microorganism infection predominates while the pathogenesis of asthma is led mainly by the different adaptive immune responses, in many cases it is difficult to identify which one is the underlying condition.
Identifying bronchiectasis in severe asthma patients and achieving a better understanding of the inflammatory phenotypes and the underlying mechanism is therefore of key importance in precision medicine.
The primary objective of the present thesis is to study the inflammatory phenotypes of asthma patients with bronchiectasis. We also aim to quantify the expression of proinflammatory and remodelling cytokines in asthma patients with and without bronchiectasis, to assess the prevalence of bronchiectasis in patients with severe asthma, and to study the impact of bronchiectasis on the clinical manifestation of asthma.
In summary, we can conclude that the prevalence of bronchiectasis is high in asthma patients, especially in those with severe asthma. In these patients, age of asthma onset and exacerbations were independent factors associated with the occurrence of bronchiectasis. The type of inflammation in asthma patients did not differ according to the presence or absence of bronchiectasis. Airway remodelling activation was observed, with increased levels of transforming growth factor beta1 (TGFβ1) and vascular endothelial growth factor (VEGF) cytokines in asthma patients with bronchiectasis.
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