Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying Campylobacter’s immediate response to Ery treatment.
Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying Campylobacter’s immediate response to Ery treatment.
Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying Campylobacter’s immediate response to Ery treatment.
Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying CampylobacterM-bM-^@M-^Ys immediate response to Ery treatment. The design utilized an available two color microarray slide for the entire transcriptome of Campylobacter jejuni wild type strain NCTC 11168. One hybridizations were performed: sham-treated NCTC 11168 v.s. lethal dose erythromycin treated NCTC 11168. Samples were independently grown and harvested. There were three biological replicates of each sample.
Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying CampylobacterM-bM-^@M-^Ys immediate response to Ery treatment. The design utilized an available two color microarray slide for the entire transcriptome of Campylobacter jejuni wild type strain NCTC 11168. One hybridizations were performed: sham-treated NCTC 11168 v.s. sub-lethal dose erythromycin treated NCTC 11168. Samples were independently grown and harvested. There were three biological replicates of each sample.
Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying CampylobacterM-bM-^@M-^Ys immediate response to Ery treatment. The design utilized an available two color microarray slide for the entire transcriptome of Campylobacter jejuni macrolide resistant strain JL272. One hybridizations were performed: sham-treated JL272 v.s. lethal dose erythromycin treated JL272. Samples were independently grown and harvested. There were three biological replicates of each sample.
Project description:Campylobacter spp. cause food-borne illnesses worldwide due to contaminated food and cross-contamination. This is at least partly the result of Campylobacter resistance in the food production chain, as modern food production facilitates the emergence and spread of resistance through intensive use of antimicrobials and international trade in raw materials and food products. The biofilm 'lifestyle' of Campylobacter contributes to this spread as it enables them to withstand stress in the environment both outside and inside the host. Campylobacter adhesion and biofilm formation has major implications for the food industry, where biofilms can be persistent sources of contamination. In our study, we described how the proteome of C. jejuni is affected by the deletion of the luxS gene on the planktonic cell type of C. jejuni, which is the first step of biofilm formation. In C. jejuni, the presence of the luxS gene has been associated with several phenotypes, including intercellular signalling, motility, biofilm formation, host colonisation, virulence, autoagglutination, cellular adherence and invasion, oxidative stress and chemotaxis. Deletion of the luxS gene is associated with a reduction or absence of the above properties compared to wild type (Elvers and Park, 2002; Guerry et al., 2006; He et al., 2008; Jeon et al., 2003; Quiñones et al., 2009; Plummer et al., 2011; Plummer, 2012; Reeser et al., 2007).
