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The work described in this thesis focusses on improving knowledge on the pathophysiology and diagnostic tools for patients with the paediatric lung diseases bronchopulmonary dysplasia (BPD) and Congenital Pulmonary Airway Malformation (CPAM). In chapter 1 we introduce BPD and CPAM, two paediatric lung diseases which have different knowledge gaps in the pathophysiology of the disease. <br/><br/>Briefly, BPD is a severe outcome in preterm infants linked to disrupted lung development and leading to chronic respiratory complications later in life, such as early-onset emphysema and asthma. Current treatment for early stage BPD patients and for patients with chronic lung complications are limited. Interestingly, premature born children that receive antibiotics have a higher chance to develop BPD complications. To better understand disease progression and to improve therapeutic options, it is imperative to understand the underlying causes. The impact of hyperoxia on lung development is widely studied and led to an experimental mouse model for BPD. However, the impact of antibiotics on lung development in the mouse BPD model has not been studied. We hypothesized that dysbiosis, resulting from antibiotics exposure, may disrupt the inflammatory and tissue repair response to oxygen exposure.<br/><br/>CPAM is the most common congenital lung anomaly, and presents as cystic structures filled with air or fluid, arising from bronchial cells during neonatal lung development. Symptomatic patients are operated to remove the cystic structure, but approximately 75% of these patients are asymptomatic at birth. At the moment, there is a lack of consensus on the management of this asymptomatic group of patients, either resect the cystic structure, potentially leading to surgical complications, or not, with the risk of infection and malignancy later in life. Our overall aim is to improve decision making on the treatment strategy of these asymptomatic patients by identifying biomarkers that could aid in this process.<br/>