S. Molin

Macrolide resistance through uL4 and uL22 ribosomal mutations in Pseudomonas aeruginosa

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.

Cystic fibrosis systemic immune profile is associated with lung microbes and characterized by widespread alterations in the innate and adaptive immune compartments

This study identifies a specific immune profile in cystic fibrosis patients linked to lung microbiota and immune dysregulation, offering potential targets for treatment.

Efflux pump mutations in Pseudomonas aeruginosa cause low-level clinical resistance and high-level tolerance to antibiotics in patients

This study shows that mexZ mutations in Pseudomonas aeruginosa lead to antibiotic tolerance and altered colonization in human airway models through overexpression of lecA.

Adaptive evolution of P. aeruginosa in human airways shows phenotypic convergence despite diverse patterns of genomic changes

This study tracks Pseudomonas aeruginosa evolution in 9 cystic fibrosis patients over decades, finding phenotypic convergence despite genomic divergence and reduced virulence features.

Detuning of the Ribosome Conformational Landscape Promotes Antibiotic Resistance and Collateral Sensitivity

The paper identifies a ribosome mutation that causes antibiotic resistance by altering conformational dynamics and reveals new tobramycin binding sites, leading to collateral sensitivity to chloramphenicol.

Metabolic specialization drives reduced pathogenicity in Pseudomonas aeruginosa CF clinical isolates

This study shows that metabolic adaptations in Pseudomonas aeruginosa clinical isolates reduce pathogenicity and virulence in cystic fibrosis patients.

Core and accessory effectors of type VI secretion systems contribute differently to the intraspecific diversity of Pseudomonas aeruginosa

The paper examines T6SS effectors in Pseudomonas aeruginosa, identifying core and accessory effectors and their roles in bacterial killing and virulence.

Macrolide therapy in Pseudomonas aeruginosa infections causes uL4 ribosomal protein mutations leading to high-level resistance

Long-term evolution of antibiotic persistence in P. aeruginosa lung infections

This study examines the long-term evolution of antibiotic persistence in P. aeruginosa lung infections over forty years, finding persistence is under positive selection and can lead to resistance, but varies by clone and antibiotic.

Development of antibiotic resistance reveals diverse evolutionary pathways to face the complex and dynamic environment of a long-term treated patient

This study tracks the long-term evolution of antibiotic-resistant Pseudomonas aeruginosa in a cystic fibrosis patient, revealing diverse genetic changes that enhance resistance to multiple cephalosporins.

Gene loss and acquisition in lineages of bacteria evolving in a human host environment

The paper analyzes gene loss and acquisition in 45 Pseudomonas aeruginosa lineages from cystic fibrosis patients over years of infection, identifying convergent evolution and virulence-related genes.

Bacterial persisters in long-term infection: emergence and fitness in a complex host environment

This study identifies high-persister (Hip) variants in Pseudomonas aeruginosa from CF patients, showing their increased fitness and role in long-term infections despite antibiotic susceptibility.

Hypermutator Pseudomonas aeruginosa exploits multiple genetic pathways to develop multidrug resistance during long term infections in the airways of cystic fibrosis patients

This study shows how hypermutator Pseudomonas aeruginosa strains develop multidrug resistance through parallel evolution of distinct genetic pathways during chronic cystic fibrosis infections.

Evolutionary highways to persistent bacterial infection

The paper analyzes longitudinal Pseudomonas aeruginosa isolates from cystic fibrosis patients to map evolutionary trajectories of infection persistence.

Privatisation rescues function following loss of cooperation

The paper shows that loss of cooperation in bacterial populations can be rescued by the evolution of private, selfish behaviors that restore essential functions.