Søren Molin

This study shows that antibiotic selection in a human airway tissue model of Pseudomonas aeruginosa leads to evolution of less virulent, tissue-preserving infections with enhanced survival.

The paper uses a human airway model to study co-infection dynamics between Staphylococcus aureus and Pseudomonas aeruginosa, revealing strain-specific traits and secretion systems that influence microbial competition.

This study shows that macrophages alter cytokine responses and bacterial spatial organization in airway epithelial cultures without changing bacterial burden.

This study shows that OprD mutations in Pseudomonas aeruginosa enhance bacterial attachment and translocation across airway epithelial barriers, altering infection dynamics beyond antibiotic resistance.

This study shows that removing glycosaminoglycans from extracellular vesicles increases their uptake and cargo delivery to target cells, suggesting glycan structures can be tuned for better drug delivery.

This paper develops a dual-cell air-liquid interface model to study epithelial-immune interactions during airway infection, finding that macrophages modulate inflammation and bacterial distribution.

The paper identifies pyruvate cross-feeding as a mechanism enabling Pseudomonas aeruginosa persistence in chronic infections by modulating host immune responses and oxidative stress.

This study uses fluorescent reporters to analyze Pseudomonas aeruginosa growth activity in human airway epithelial models, revealing strain-specific colonization patterns and growth hierarchies across infection niches.

The paper investigates infection dynamics and virulence of Pseudomonas aeruginosa in human airway epithelial models, identifying four infection clusters based on strain-specific virulence and host response.

This study shows that macrolides are effective against Pseudomonas aeruginosa in airway infections but lead to resistance via uL4 and uL22 ribosomal mutations, requiring higher antibiotic concentrations and reducing bacterial fitness.