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Pathoblockers Against P. Aerugainosa May Soon Be Developed

Researchers discovered the enzyme responsible for producing a biofilm that shields Pseudomonas aeruginosa from immune cells and antibiotics.

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        A clinically relevant pathogen may soon succumb to antibiotics and immune cells after researchers discovered its Achilles heel. 

        Highlighted in the journal Proceedings of the National Academy of Sciences, the study focused on Pseudomonas aeruginosa, which is known for its life-threatening infections that can lead to a high mortality rate. 

        Researchers from the Centre for Experimental and Clinical Infection Research in Hannover (TWINCORE) and Helmholtz Centre for Infection Research (HZI) identified the enzyme responsible for modifying tRNA molecules. Called GidA, this enzyme controls the virulence of P. aeruginosa and the pathogen's ability to produce formidable biofilm communities that render various antibiotics and immune cells ineffective.

        Dr. Nicolas Oswaldo Gomez, HZI scientist and one of the first authors of the study, said they explored the effects of removing GidA's ability to modify tRNAs and investigated the resulting impact on bacterial pathogenicity:

        "In all experiments, pathogenicity was significantly reduced compared to the wild type. If GidA is not present, some tRNA molecules are no longer modified, which obviously means that proteins that are crucial for pathogenicity are no longer produced. In further investigations, for example, we were able to determine that the structure of the biofilm was altered and that a quinolone antibiotic was significantly more effective than in the wild type."

        Prof. Susanne Häußler, head of the Institute for Molecular Bacteriology at TWINCORE AND HZI, said the results proved promising for developing pathoblockers. Unlike antibiotics that are designed to eliminate pathogens, pathoblockers only weaken the pathogenic effect:

        "The results of our study make it clear that the pathogenicity of Pseudomonas aeruginosa is subject to a specialised epigenetic control process in which GidA functions like a kind of overriding switch. And we can and should utilise this - as a starting point for the development of effective pathoblockers against Pseudomonas aeruginosa and other highly problematic bacterial pathogens."

        Read the full article here to learn more about the methods researchers used in this study.

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