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<jats:title>Abstract</jats:title><jats:p><jats:italic>Campylobacter</jats:italic> is the leading cause of bacterial foodborne gastroenteritis in many countries. Source attribution studies unequivocally identify the handling or consumption of contaminated poultry meat as the primary risk factor. One potential strategy to control <jats:italic>Campylobacter</jats:italic> is to select poultry with increased resistance to colonisation. We conducted genomic and transcriptomic analyses of commercial pedigree broilers exposed to <jats:italic>Campylobacter</jats:italic> to examine persistent colonisation of the caecum as a quantitative trait. 3,000 broilers were genotyped using a 50K single nucleotide polymorphism (SNP) array and imputed to 600K SNPs. Genotypes were analysed for associations with the number of viable <jats:italic>Campylobacter</jats:italic> in the caeca. Heritability of the trait was modest but significantly greater than zero (h<jats:sup>2</jats:sup>=0.11 ± 0.03). Genome-wide association analyses confirmed quantitative trait loci (QTL) on chromosomes 14 and 16 previously identified using the progeny of crosses of inbred lines differing in resistance, and detected two additional genome-wide significant QTLs on chromosomes 19 and 26. RNA-Seq analysis of the transcriptome of caecal tonsils from birds at the low and high extremes of <jats:italic>C. jejuni</jats:italic> colonisation phenotype identified differentially transcribed genes, mainly located within the QTL on chromosome 16 and proximal to the major histocompatibility complex (MHC) locus. We also identified strong <jats:italic>cis</jats:italic>-QTLs located within the MHC suggesting the presence of <jats:italic>cis</jats:italic>-acting variation in both MHC class I, class II and BG genes. Multiple other <jats:italic>cis-</jats:italic>acting variants were identified in association with key immune genes (<jats:italic>COPS3, CCL4, CR1L, C4BP, PLGR</jats:italic>) in the other QTLs. Pathway and network analysis implicated cooperative functional pathways and networks in colonisation, including those related to antigen presentation, innate and adaptive immune responses, calcium, and renin-angiotensin signalling. While co-selection for enhanced resistance and other breeding goal traits is feasible, the frequency of resistance-associated alleles was high in the population studied and non-genetic factors significantly influence <jats:italic>Campylobacter</jats:italic> colonisation in poultry.</jats:p><jats:sec><jats:title>Author summary</jats:title><jats:p><jats:italic>Campylobacter</jats:italic> infection is estimated to cause 95 million illnesses in people worldwide each year. Human infections mostly involve gastroenteritis, but can have severe complications. The handling or consumption of contaminated poultry meat is a key risk factor for human campylobacteriosis. The bacteria reach high numbers in the intestines of chickens reared for meat (broilers) and are frequently found on carcasses after slaughter. Effective vaccines against <jats:italic>Campylobacter</jats:italic> are not yet available, and treatments to reduce carcass contamination (e.g. chlorination) are not acceptable in some markets. One alternative is to breed for chickens with improved resistance to <jats:italic>Campylobacter</jats:italic> colonisation. To test the feasibility of this option in commercial birds, we analysed the genetic make-up of 3,000 pedigree broilers and determined the number of <jats:italic>Campylobacter</jats:italic> in their gut. There were associations between specific regions of the chicken genome and resistance to <jats:italic>Campylobacter</jats:italic>. Within some of these regions, expression of certain genes differed between birds at the low and high extremes of <jats:italic>Campylobacter</jats:italic> colonisation, providing a potential explanation for genetic variation in resistance. Selection of poultry with increased resistance to <jats:italic>Campylobacter</jats:italic> colonisation may be a complementary strategy to improved biosecurity, management, handling and processing procedures to reduce the burden of <jats:italic>Campylobacter</jats:italic> on human health.</jats:p></jats:sec>

Original publication

DOI

10.1101/2020.04.14.040832

Type

Journal article

Publisher

Cold Spring Harbor Laboratory

Publication Date

15/04/2020