Genetic control ofCampylobactercolonisation in broiler chickens: genomic and transcriptomic characterisation
Authors: Psifidi Androniki , Kranis Andreas , Rothwell Lisa M. , Bremner Abi , Russell Kay , Robledo Diego , Bush Stephen J. , Fife Mark , Hocking Paul M. , Banos Georgios , Hume David A. , Kaufman Jim , Bailey Richard A. , Avendano Santiago , Watson Kellie A. , Kaiser Pete , Stevens Mark. P. 
Published: April 2020

AbstractCampylobacteris 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 controlCampylobacteris to select poultry with increased resistance to colonisation. We conducted genomic and transcriptomic analyses of commercial pedigree broilers exposed toCampylobacterto 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 viableCampylobacterin the caeca. Heritability of the trait was modest but significantly greater than zero (h2=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 ofC. jejunicolonisation 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 strongcis-QTLs located within the MHC suggesting the presence ofcis-acting variation in both MHC class I, class II and BG genes. Multiple othercis-acting variants were identified in association with key immune genes (COPS3, CCL4, CR1L, C4BP, PLGR) 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 influenceCampylobactercolonisation in poultry.Author summaryCampylobacterinfection 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 againstCampylobacterare 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 toCampylobactercolonisation. 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 ofCampylobacterin their gut. There were associations between specific regions of the chicken genome and resistance toCampylobacter. Within some of these regions, expression of certain genes differed between birds at the low and high extremes ofCampylobactercolonisation, providing a potential explanation for genetic variation in resistance. Selection of poultry with increased resistance toCampylobactercolonisation may be a complementary strategy to improved biosecurity, management, handling and processing procedures to reduce the burden ofCampylobacteron human health.