Campylobacter jejuni: collective components promoting a successful enteric lifestyle

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Abstract

<p class="first" id="d3843071e69">Campylobacter jejuni is the leading cause of bacterial diarrhoeal disease in many areas of the world. The high incidence of sporadic cases of disease in humans is largely due to its prevalence as a zoonotic agent in animals, both in agriculture and in the wild. Compared with many other enteric bacterial pathogens, C. jejuni has strict growth and nutritional requirements and lacks many virulence and colonization determinants that are typically used by bacterial pathogens to infect hosts. Instead, C. jejuni has a different collection of factors and pathways not typically associated together in enteric pathogens to establish commensalism in many animal hosts and to promote diarrhoeal disease in the human population. In this Review, we discuss the cellular architecture and structure of C. jejuni, intraspecies genotypic variation, the multiple roles of the flagellum, specific nutritional and environmental growth requirements and how these factors contribute to in vivo growth in human and avian hosts, persistent colonization and pathogenesis of diarrhoeal disease. </p>

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Influence of the Gut Microbiota Composition on Campylobacter jejuni Colonization in Chickens

Zifeng Han, Thomas Willer, Li Li … (2017)

ABSTRACT The Campylobacter jejuni-host interaction may be affected by the host's gut microbiota through competitive exclusion, metabolites, or modification of the immune response. To understand this interaction, C. jejuni colonization and local immune responses were compared in chickens with different gut microbiota compositions. Birds were treated with an antibiotic cocktail (AT) (experiments 1 and 2) or raised under germfree (GF) conditions (experiment 3). At 18 days posthatch (dph), they were orally inoculated either with 104 CFU of C. jejuni or with diluent. Cecal as well as systemic C. jejuni colonization, T- and B-cell numbers in the gut, and gut-associated tissue were compared between the different groups. Significantly higher numbers of CFU of C. jejuni were detected in the cecal contents of AT and GF birds, with higher colonization rates in spleen, liver, and ileum, than in birds with a conventional gut microbiota (P < 0.05). Significant upregulation of T and B lymphocyte numbers was detected in cecum, cecal tonsils, and bursa of Fabricius of AT or GF birds after C. jejuni inoculation compared to the respective controls (P < 0.05). This difference was less clear in birds with a conventional gut microbiota. Histopathological gut lesions were observed only in C. jejuni-inoculated AT and GF birds but not in microbiota-colonized C. jejuni-inoculated hatchmates. These results demonstrate that the gut microbiota may contribute to the control of C. jejuni colonization and prevent lesion development. Further studies are needed to identify key players of the gut microbiota and the mechanisms behind their protective role.