Project description:Campylobacter jejuni is a common cause of diarrheal disease worldwide. Human infection typically occurs through the ingestion of contaminated poultry products. We previously demonstrated that an attenuated Escherichia coli live vaccine strain expressing the C. jejuni N-glycan on its surface reduces the Campylobacter load in more than 50% of vaccinated leghorn and broiler birds to undetectable levels (responder birds), whereas the remainder of the animals were still colonized (non-responders). To understand the underlying mechanism, we conducted 3 larger scale vaccination and challenge studies using 135 broiler birds and found a similar responder/non responder effect. The submitted data were used for a genome-wide association study of the chicken responses to glycoconjugate vaccination against Campylobacter jejuni.
Project description:Chromosomal structural variation can cause alterations in gene dosage and gene regulation between genomes. Structural variants producing a change in the number of copies of a genomic region are termed copy number variants (CNVs). CNVs have been demonstrated to have causative effects on both Mendelian and complex traits, including susceptibility to infectious diseases. We are interested in mapping CNVs to domesticated chicken breeds to help determine structural variation between genomes that influences economically important traits. For this study, Fayoumi, Leghorn, Line A broiler and Line B broiler chicken were chosen. Fayoumi and Leghorn chickens were selected as these two breeds harbor different responses certain pathogens like Avian Influenza Virus and coccidiosis; Broiler Line A and Line B indivduals were chosen as they harbor different intestinal colonization loads to the bacterium Campylobacter jejuni. Campylobacter genetic Line A and genetic Line B are from a commercial producer have been previously described as either resistant (Line A) or susceptible (Line B). Highly inbred chicken lines Fayoumi M15.2 (n=6) and Leghorn GHs6 (n=6) and broilers from Line A (n=24 individuals in pools of 4) and Line B (n=24 individuals in pools of 4)were subjected to array Comparative Genomic Hybridization (aCGH). Each sample was normalized to a Red Jungle Fowl reference. CNVs for each individual and between lines were determined. The major goal of this study was to discover and characterize CNVs in chickens to further narrow in on Quantitative Trait Loci (QTLs) affecting disease response.
Project description:Fluoroquinolones (FQs) are one class of commonly used antimicrobials in clinical therapy of diseases caused by Campylobacter and other foodborne pathogens. The molecular mechanisms underlying the response of Campylobacter to FQ treatment is of interest because unlike other enteric bacteria, Campylobacter lacks many genes encoding components of DNA repair systems and SOS response. To understand how Campylobacter survive antibiotic treatment, DNA microarray was used to compare the gene expression profiles of C. jejuni 11168 in the presence and absence of ciprofloxacin. Our analysis identified 45 genes that showed ≥1.5-fold (p<0.05) changes in expression in the presence of ciprofloxacin. The up-regulated genes (13) are involved in cell membrane biosynthesis and DNA repair or have unknown functions, while the majority of the down-regulated genes (32) are involved in cellular process and energy metabolism. These findings suggest that C. jejuni modulates membrane biosynthesis, increases spontaneous mutation rates, and decreases metabolism in response to fluoroquinolone treatment. Keywords: 0.06 µg/ml (0.5X MIC) or 1.2 µg/ml (10X MIC) ciprofloxacin treated campylobacter VS. untreated campylobacter, the bacterial cells were treated for 0.5 hour
Project description:Comparsion of proteomes of Campylobacter fetus subsp. fetus to compare protein level via iBAQ analysis, expression (by LFQ) and coverage between Campylobacter fetus subsp. fetus strain82-40 vs Campylobacter fetus subsp. fetus strain ATCC 27374
Project description:Campylobacter jejuni is the most prevalent cause of foodborne bacterial enteritis worldwide. This study aims at the characterisation of pathomechanisms and signalling in Campylobacter-induced diarrhoea in the human mucosa. During routine colonoscopy, biopsies were taken from patients suffering from campylobacteriosis. RNA-seq of colon biopsies was performed to describe Campylobacter jejuni-mediated effects. Mucosal mRNA profiles of acutely infected patients and healthy controls were generated by deep sequencing using Illumina HiSeq 2500. This data provide the basis for subsequent upstream regulator analysis.