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Worldwide Campylobacter jejuni is a leading cause of foodborne disease. Contamination of chicken meat with digesta from C. jejuni -positive birds during slaughter and processing is a key route of transmission to humans through the food chain. Colonization of chickens with C. jejuni elicits host innate immune responses that may be modulated by dietary additives to provide a reduction in the number of campylobacters colonizing the gastrointestinal tract and thereby reduce the likelihood of human exposure to an infectious dose. Here we report the effects of prebiotic galacto-oligosaccharide (GOS) on broiler chickens colonized with C. jejuni when challenged at either an early stage in development at 6 days of age or 20 days old when campylobacters are frequently detected in commercial flocks. GOS-fed birds had increased growth performance, but the levels of C. jejuni colonizing the cecal pouches were unchanged irrespective of the age of challenge. Dietary GOS modulated the immune response to C. jejuni by increasing cytokine IL-17A expression at colonization. Correspondingly, reduced diversity of the cecal microbiota was associated with Campylobacter colonization in GOS-fed birds. In birds challenged at 6 days-old the reduction in microbial diversity was accompanied by an increase in the relative abundance of Escherichia spp. Whilst immuno-modulation of the Th17 pro-inflammatory response did not prevent C. jejuni colonization of the intestinal tract of broiler chickens, the study highlights the potential for combinations of prebiotics, and specific competitors (synbiotics) to engage with the host innate immunity to reduce pathogen burdens., (Copyright © 2020 Flaujac Lafontaine, Richards, Connerton, O’Kane, Ghaffar, Cummings, Fish and Connerton.)

Campylobacter contaminated poultry meat is a major source of human foodborne illness. Campylobacter coli strain OR12 is a robust colonizer of chickens that was previously shown to outcompete and displace other Campylobacter strains from the chicken's gastrointestinal tract. This strain is capable of aerobic growth on blood agar. Serial aerobic passage increased this aerotolerance as assessed by quantitative assays for growth and survival on solid media. Aerotolerance was also associated with increased peroxide stress resistance. Aerobic passage did not alter cellular morphology or motility or hinder the microaerobic growth rate. Colonization of broiler chickens by aerotolerant C. coli OR12 was significantly lower than the wild-type strain at 3 days after challenge but not by 7 days, suggesting adaptation had occurred. Bacteria recovered from chickens had retained their aerotolerance, indicating this trait is stable. Whole genome sequencing enabled comparison with the wild-type sequence. Twenty-three point mutations were present, none of which were in genes known to affect oxidative stress resistance. Insertions or deletions caused frame shifts in several genes including, phosphoglycerate kinase and the b subunit of pyruvate carboxylase that suggest modification of central and carbohydrate metabolism in response to aerobic growth. Other genes affected include those encoding putative carbonic anhydrase, motility accessory factor, filamentous haemagglutinin, and aminoacyl dipeptidase proteins. Aerotolerance has the potential to affect environmental success and survival. Increased environmental survival outside of the host intestinal tract may allow opportunities for transmission between hosts. Resistance to oxidative stress may equate to increased virulence by virtue of reduced susceptibility to oxidative free radicals produced by host immune responses. Finally, resistance to ambient atmospheric oxygen may allow increased survival on chicken skin, and therefore constitutes an increased risk to public health.