ASU researcher part of team discovering ways to fight drug-resistant bacteria
3D model used for the team's research. Photo courtesy of Banu Ozkan
A new study published in the Science Advances journal featuring Arizona State University researchers has found vulnerabilities in certain strains of bacteria that are antibiotic resistant, just as new projections predict deaths caused by drug-resistant infections could surge to 2 million per year by 2050.
The interdisciplinary team included the Department of Physics’ Ozkan Lab, the Ojalvo Lab at the Universitat Pompeu Fabra in Spain and the Suel Lab at the University of California San Diego. Their motivation for the investigation came from the question of why mutant, drug-resistant variants of bacteria don’t multiply and dominate populations.
The team discovered that a physiological limitation hinders the ability for antibiotic-resistant bacteria to take over — a key component that can potentially be exploited in prohibiting the spread of antibiotic resistance.
Ozkan Lab Director and Professor Banu Ozkan led atomic-scale modeling to observe ribosomes and their relation to magnesium ions. When looking at the ribosome variant within the bacterium Bacillus subtilis, or “L22,” researchers saw that competition for magnesium hinders the growth of L22 more than a “wild-type,” or normal, nonresistant ribosome.
They demonstrated that mutant antibiotic-resistant ribosome variants were competing for magnesium ions with adenosine triphosphate molecules, a source of energy for cells.
“Our study has uncovered a fascinating discovery: Antibiotic-resistant strains of bacteria depend more heavily on magnesium than we previously thought. This magnesium reliance creates a limitation that prevents the bacteria from becoming more dominant,” Ozkan said.
“The team’s findings open the door to new ways to prevent antibiotic resistance without relying on drugs or harmful chemicals.”
For example, it could be possible to chelatea form of bonding of ions and their molecules to metal ions magnesium ions from bacterial environments, inhibiting resistant strains without impacting wild-type bacteria, which is beneficial to human health.
“Because different cellular processes compete for these limited metal ions, we believe that managing this competition could create unexpected connections between different cellular functions,” Ozkan said.
“By controlling the available metal ions, we can influence and even change how the cell behaves — offering a powerful new tool in the fight against antibiotic resistance.”
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