Imagine trying to settle into a new home while constantly being attacked. That's what the bacterium Pseudomonas aeruginosa faces when it infects the lungs, and it can't both spread and protect itself from antibiotics at the same time.
Ecole Polytechnique Fédérale de LausanneOct 25 2024 Imagine trying to settle into a new home while constantly being attacked. That's what the bacterium Pseudomonas aeruginosa faces when it infects the lungs, and it can't both spread and protect itself from antibiotics at the same time.
New research by the group of Alexandre Persat at EPFL's Global Health Institute has now uncovered how P. aeruginosa manages the trade-off between colonizing and surviving during infection by switching between biofilm formation for antibiotic protection and a more mobile, "planktonic" state to spread and access nutrients, depending on the environmental pressures they face. The study is published in Nature Microbiology.
Thanks to the Tn-seq technique, the scientists identified which genes were important for the bacterium's survival under different conditions: those which contributed to fitness during mucosal colonization and those which helped the bacteria tolerate antibiotics. Related StoriesWhat Persat's team uncovered is the mechanism behind this dilemma. They found that biofilm formation imposes a "metabolic burden," meaning that producing the sticky matrix that holds the biofilm together consumes resources, slowing down the bacteria's ability to spread. In experiments, bacteria that couldn't form biofilms spread more efficiently but were left vulnerable to antibiotics.
Antibiotic Antibiotic Resistance Bacteria Biofilms Bronchiectasis Cystic Fibrosis Fibrosis Hospital Lungs Microbiology Nutrients Physiology
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