Publications by authors named "Draginja Kovacevic"

Serine proteases are important regulators of airway epithelial homeostasis. Altered serum or cellular levels of two serpins, Scca1 and Spink5, have been described for airway diseases but their function beyond antiproteolytic activity is insufficiently understood. To close this gap, we generated fly lines with overexpression or knockdown for each gene in the airways.

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The airway epithelial cells and overlying layer of mucus are the first point of contact for particles entering the lung. The severity of environmental contributions to pulmonary disease initiation, progression, and exacerbation is largely determined by engagement with the airway epithelium. Despite the cellular cross-talk and cargo exchange in the microenvironment, epithelial cells produce miRNAs associated with the regulation of airway features in asthma.

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Airway remodeling is an umbrella term for structural changes in the conducting airways that occur in chronic inflammatory lung diseases such as asthma or chronic obstructive pulmonary disease (COPD). The pathobiology of remodeling involves multiple mesenchymal and lymphoid cell types and finally leads to a variety of hardly reversible changes such as hyperplasia of goblet cells, thickening of the reticular basement membrane, deposition of collagen, peribronchial fibrosis, angiogenesis and hyperplasia of bronchial smooth muscle cells. In order to develop solutions for prevention or innovative therapies, these complex processes must be understood in detail which requires their deconstruction into individual building blocks.

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Early life exposures to antibiotics negatively impact respiratory health and are associated with an increased risk of childhood asthma. It is explained that the lung is inclined to develop chronic inflammatory phenotypes due to early antibiotic alteration in the gut microbiome. We investigated whether a gut-targeted antibiotic has an impact on the lung microbiome and on pulmonary immunity.

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Article Synopsis
  • Early exposure to cigarette smoke (CS) disrupts lung development processes, increasing the risk of chronic respiratory diseases like asthma and COPD later in life.
  • Using Drosophila melanogaster larvae, researchers found that CS activates specific genes that respond to stress and affects various biological pathways related to immune response and development in both sexes, with some effects being gender-specific.
  • CS exposure also led to higher mortality rates and decreased growth metrics in male larvae compared to controls, highlighting the significant impact of early environmental stressors on lung health and development.
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To examine the role of smoking on the bacterial community composition of the upper and the lower respiratory tract, a monocentric, controlled prospective study was performed, including healthy smokers, ex-smokers and never-smokers. Smokers were further grouped according to their smoking history. Bacterial diversity was analysed using a molecular barcoding approach based on directly extracted DNA.

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Article Synopsis
  • Smokers with "healthy" lungs experience more severe respiratory infections, but the reasons for this remain unclear.
  • A study using mice and lung cell cultures revealed that cigarette smoke exposure increases certain types of immune cells (dendritic cells) in the lungs and disrupts the protective barrier function of lung epithelial cells.
  • Additionally, smoke exposure suppressed the body's antiviral and inflammatory responses to subsequent viral infections like influenza H1N1, suggesting a heightened vulnerability in smokers.
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