Difference between revisions of "Team:Westminster UK"

 
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    Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing
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    of <i>Pseudomonas</i>
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    Hundreds of millions of patients every year acquire an infection from their
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    healthcare setting, according to the World Health Organisation. Treating
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    these nosocomial infections is complicated by antibiotic resistance; there
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    has been a rapid increase of multidrug resistance (MDR) bacteria, including
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    strains of the gram-negative genera, <i>Pseudomonas</i> and <i>Escherichia</i>.
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    Opportunistic <i>Pseudomonas</i> are responsible for 10% of all global hospital
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    acquired infections which cause disease in immuno-deficient individuals. In
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    cystic fibrosis, <i>Pseudomonas aeruginosa</i> is estimated to colonise the lungs
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    of 50-90% of patients. A major contributor to bacterial antibiotic
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    resistance is the aggregation of bacteria to form biofilms. Bacteria within
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    biofilms communicate with each other through the release of chemicals, such
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    as N-Acyl homoserine lactones (AHL), these quorum-sensing molecules are
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    essential to biofilm formation. This project will aim to develop strategies
 +
    to inhibit biofilm formation by targeting the specific genes responsible
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    for AHL regulation; ppuR, ppuI and RsaL in <i>Pseudomonas putida</i>. This
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    project has a vast range of potential therapeutic applications such as
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    development of biocontainment devices against MDR bacteria. This project
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    will provide a fundamental contribution to understanding and combating
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    antibiotic resistance with applications for treating nosocomical infections
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<h1> Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing of Pseudomonas</h1>
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<p>Hundreds of millions of patients every year acquire nosocomial infections according to the World Health Organisation. Treatment is complicated by antibiotic resistance with a rapid increase of multi-drug resistance (MDR) bacteria, including strains of the gram-negative genera: Pseudomonas and Escherichia. Opportunistic Pseudomonas are responsible for 10% of all global nosocomial infections in immunocompromised individuals with 50-90% of patients of cystic fibrosis patients suffering from a Pseudomonas Aeruginosa infection.
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A major contributor to  antibiotic resistance is  bacterial aggregation to form biofilms. Bacteria within biofilms communicate through chemicals, such as N-Acyl homoserine lactones (AHL), quorum-sensing molecules essential to biofilm formation. We  aim to develop strategies to inhibit biofilm formation by targeting AHL regulation genes: ppuR, ppuA, ppuI and RsaL in Pseudomonas putida. This project has a vast range of potential therapeutic applications such as the development of biocontainment devices and will provide fundamental information to understanding and developing tools in combating antibiotic resistance.
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Latest revision as of 15:51, 1 November 2017

Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing of Pseudomonas

Hundreds of millions of patients every year acquire an infection from their healthcare setting, according to the World Health Organisation. Treating these nosocomial infections is complicated by antibiotic resistance; there has been a rapid increase of multidrug resistance (MDR) bacteria, including strains of the gram-negative genera, Pseudomonas and Escherichia. Opportunistic Pseudomonas are responsible for 10% of all global hospital acquired infections which cause disease in immuno-deficient individuals. In cystic fibrosis, Pseudomonas aeruginosa is estimated to colonise the lungs of 50-90% of patients. A major contributor to bacterial antibiotic resistance is the aggregation of bacteria to form biofilms. Bacteria within biofilms communicate with each other through the release of chemicals, such as N-Acyl homoserine lactones (AHL), these quorum-sensing molecules are essential to biofilm formation. This project will aim to develop strategies to inhibit biofilm formation by targeting the specific genes responsible for AHL regulation; ppuR, ppuI and RsaL in Pseudomonas putida. This project has a vast range of potential therapeutic applications such as development of biocontainment devices against MDR bacteria. This project will provide a fundamental contribution to understanding and combating antibiotic resistance with applications for treating nosocomical infections