Most people with cystic fibrosis die before age 30 because the antibiotics used to treat their lung infections stop working. The bacterium *Pseudomonas aeruginosa* is the main cause of death, and it is becoming resistant to nearly every available drug. This research aims to turn a natural bacterial weapon into a precision antibiotic. The team is working with molecules called bacteriocins—antibiotics that bacteria themselves produce to kill closely related rivals. Unlike broad-spectrum drugs that wipe out many species, these molecules target only *Pseudomonas aeruginosa* with extreme potency. The researchers have already shown the molecule works in the lab; now they need to develop methods to produce and formulate it as a safe therapeutic for humans, then run extensive safety tests. If successful, this would give clinicians a highly targeted drug that kills the infection without disrupting the rest of the lung microbiome. For people with cystic fibrosis, that could mean fewer treatment failures, longer survival, and a reduced need for last-resort antibiotics. More broadly, it demonstrates a strategy for developing antibiotics that evolution has already refined—matching a specific killer to a specific target—rather than trying to design one from scratch.
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Antibiotic resistance poses a dire threat to the population and if no new antibiotics are developed we may soon find ourselves with no useful therapeutics to treat a range of potentially fatal bacterial infections. Unfortunately, few new antibiotics have been developed in recent years and for some bacteria there are almost no therapeutic options remaining. As the prevalence of infections caused by multidrug resistant bacteria is rapidly increasing this problem may soon become a modern health crisis. A major problem in the development of antibiotics is identifying suitable molecules within bacteria to target with novel molecules. This is one reason why, even with great advances in our understanding of bacteria such as the ability to sequence their genomes, most efforts to develop new antibiotics have failed. However, in contrast to our own ability to create effective antibiotics, other microorganisms are extremely good at this. This is a direct consequence of evolution by natural selection where the ability to produce an effective antibiotic and thus kill bacteria that are competing for recourses is strongly selected for. We are working on a group of antibiotics that have evolved to kill only bacteria very closely related to the producing bacterium. Although they do not kill all bacteria, they have evolved to kill the bacteria they do target with unmatched potency. We intend to develop a highly targeted antibiotic as a therapeutic for the treatment of a specific bacterium (Pseudomonas aeruginosa) that is the major cause of death in people with cystic fibrosis (CF). Since we know exactly the type of bacteria that is responsible for these infections a highly targeted approach should work well. This is an area of great unmet clinical need, since the antibiotics that are currently used to treat these infections frequently fail and so most CF patients still die before they reach 30. The aim of this work is to develop a highly targeted antibiotic to treat Pseudomonas aeruginosa infections that we have demonstrated is highly effective against this organism. To achieve this we will develop methods to produce and formulate this molecule as a therapeutic that can be used in humans and undertake extensive safety testing to demonstrate it is safe for use by people with CF.
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