Many people have, at some point in their lives, been treated for a bacterial infection with a dose of antibiotics. This is commonly a swift and effective treatment, but sometimes a few bacteria learn to survive and become “resistant” to the antibiotic. This phenomenon, called antibiotic resistance, is a major challenge in healthcare, and researchers are constantly looking for new antibiotics to combat these evolving bacteria. Recently, a team at the University of Southern Denmark uncovered a new mechanism we could use to target such resistant bacteria.
P. aeruginosa is a bacteria that can develop antibiotic resistance by forming biofilms, which are complex communities of bacteria that together form a protective “film” that occludes antibiotics from reaching the bacteria. The researchers found a group of three genes in the P. aeruginosa bacteria that, when turned on, prevent biofilms from forming. Importantly, they also discovered that stressing the bacteria by targeting its bacterial cell wall, a unique protective layer around a bacteria, could turn these genes on and prevent biofilm formation. Since human cells do not have a bacterial cell wall, we can take an antibiotic that attacks that cell wall without worrying it would accidentally damage our own cells.
Understanding bacterial evolution is key to mitigating the negative effects of infections. Slacking on the development of new bacterial antibiotics can potentiate an epidemic or even a global pandemic. While the treatment of P. aeruginosa in patients by stressing the cell wall has yet to be tested, it opens the field to another potential treatment option that could be critical in fighting resistant bacterial infections.
This study was led by Magnus Østergaard with corresponding author Clare Kirkpatrick at the University of Southern Denmark.
Managing Correspondent: Olivia Lavidor
Press Article: Researchers thwart resistant bacteria’s strategy (Phys.org)
Original Journal Article: The uncharacterized PA3040-3042 operon is part of the cell envelope stress response and a tobramycin resistance determinant in a clinical isolate of Pseudomonas aeruginosa (Microbiology Spectrum)
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