New Drug Target Makes Superbugs Choke on Their Own Toxic Molecules

May, 2021 - By SMI

New Drug Target Makes Superbugs Choke on Their Own Toxic Molecules

Antibiotic-resistant bacteria, also known as "superbugs," are one of the most serious public-health risks. Now, University of Georgia researchers discovered a new possible vulnerability in some of the most dangerous strains, which could cause them to choke on their own toxic molecules.

Antibiotics is one of the most significant scientific breakthroughs of the twentieth century, but decades of overuse and misuse have severely harmed their efficacy. These medications have increasingly developed resistance in pathogenic bacteria. Scientists have predicted that if current trends continue, superbugs will be responsible for 10 million deaths each year by 2050.

New antibiotics are desperately needed and scientists are working on a variety of mechanisms to give themselves the best chance. Now, a team of researchers from the College of Veterinary Medicine, discovered a new process that could be targeted by potential medicines to eradicate superbugs. The research was focused on gram-negative bacteria, which are an especially dangerous type of microbe. Antibiotics have a hard time getting through these bacteria because they have two cell membranes. Furthermore, they contain toxic molecules known as lipopolysaccharides (LPS), which can trigger potentially fatal conditions such as septic shock, among other items.

Cardiolipin, a protein, was the key to the new research. To figure out what this molecule does within bacteria, the researchers genetically modified E. coli to prevent it from producing cardiolipin. It turned out that this single molecule is involved in both gram-negative defense mechanisms. The researchers discovered that E. coli could no longer move the toxic LPS from its core to the cell surface without cardiolipin. Instead, poisonous molecules build up within the bacterium until it bursts open, killing it. Those that do live would have damaged outer membranes, making it easier for current antibiotics to kill them.

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