Abstract
There are still major gaps in our understanding of the bacterial factors that influence the outcomes of human Campylobacter jejuni infection. The aim of this study was to compare the virulence-associated features of 192 human C. jejuni strains isolated from hospitalized patients with diarrhoea (150/192, 78.1%), bloody diarrhoea (23/192, 11.9%), gastroenteritis (3/192, 1.6%), ulcerative colitis (3/192, 1.5%), and stomach ache (2/192, 1.0%). Traits were analysed with genotypic and phenotypic methods, including PCR and extracellular matrix protein (ECMP) binding, adhesion, and invasion capacities. Results were studied alongside patient symptoms, but no distinct links with them could be determined. Since the capacity of C. jejuni to invade host epithelial cells is one of its most enigmatic attributes, a high throughput transcriptomic analysis was performed in the third hour of internalization with a C. jejuni strain originally isolated from bloody diarrhoea. Characteristic groups of genes were significantly upregulated, outlining a survival strategy of internalized C. jejuni comprising genes related (1) to oxidative stress; (2) to a protective sheath formed by the capsule, LOS, N-, and O- glycosylation systems; (3) to dynamic metabolic activity supported by different translocases and the membrane-integrated component of the flagellar apparatus; and (4) to hitherto unknown genes.
Highlights
Campylobacter jejuni is regarded as a major cause of diarrhoeal diseases in both industrialised and developing countries, mostly associated with the consumption of undercooked poultry meat and contaminated surface water [1]
Isolates were grown on Charcoal Cefoperazone Deoxycholate Agar (CCDA) at 42 ◦C under microaerophilic conditions generated by the MACS–MICS jar-system (Don Whitley Scientific, Shipley, UK)
Despite its importance as a zoonotic agent and the availability of more than 1600 assembled genomes (NCBI genome database), there is an incomplete understanding of C. jejuni pathogenesis
Summary
Campylobacter jejuni is regarded as a major cause of diarrhoeal diseases in both industrialised and developing countries, mostly associated with the consumption of undercooked poultry meat and contaminated surface water [1]. The clinical spectrum of campylobacteriosis ranges from asymptomatic to severe symptoms, such as bloody diarrhoea, sometimes embodied in post-infection sequelae, including Miller–Fisher and Guillain–Barré syndromes [4,5]. To reduce and prevent Campylobacter infections in humans, it is crucial to understand those virulence factors and molecular mechanisms that directly contribute to pathogenesis. There are still major gaps in our understanding, the roles of major virulence properties, including its chemotaxis, motility, spiral shape, adhesion, and invasion abilities, are known. Numerous studies have documented the prevalence of specific coding regions in pathogenicity-associated features in human and animal isolates and examined correlations between their presence in the bacterial genome and disease severity [1,6,7,8,9], with controversial results
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