Difference between revisions of "Team:Westminster UK/Test"
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| − | <h1> Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing of Pseudomonas</ | + | <h1> Abstract </h1> |
| + | <h2> Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing of Pseudomonas</h2> | ||
<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. | <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. | ||
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. | 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. | ||
Revision as of 14:33, 13 October 2017
WELCOME TO THE BIO BUSTERS
Abstract
Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing of Pseudomonas
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. 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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