Abstract
Campylobacter jejuni is a leading cause of foodbourne gastroenteritis, despite fragile behaviour under standard laboratory conditions. In the environment, C. jejuni may survive within biofilms, which can impart resident bacteria with enhanced stress tolerance compared to their planktonic counterparts. While C. jejuni forms biofilms in vitro and in the wild, it had not been confirmed that this lifestyle confers stress tolerance. Moreover, little is understood about molecular mechanisms of biofilm formation in this pathogen. We previously found that a ΔcprS mutant, which carries a deletion in the sensor kinase of the CprRS two-component system, forms enhanced biofilms. Biofilms were also enhanced by the bile salt deoxycholate and contained extracellular DNA. Through more in-depth analysis of ΔcprS and WT under conditions that promote or inhibit biofilms, we sought to further define this lifestyle for C. jejuni. Epistasis experiments with ΔcprS and flagellar mutations (ΔflhA, ΔpflA) suggested that initiation is mediated by flagellum-mediated adherence, a process which was kinetically enhanced by motility. Lysis was also observed, especially under biofilm-enhancing conditions. Microscopy suggested adherence was followed by release of eDNA, which was required for biofilm maturation. Importantly, inhibiting biofilm formation by removal of eDNA with DNase decreased stress tolerance. This work suggests the biofilm lifestyle provides C. jejuni with resilience that has not been apparent from observation of planktonic bacteria during routine laboratory culture, and provides a framework for subsequent molecular studies of C. jejuni biofilms.
Highlights
Campylobacter jejuni is a prevalent food- and waterborne gastrointestinal pathogen
We previously noted extracellular DNA in C. jejuni biofilms, and thatthe amount of eDNA appeared to be qualitatively increased in strains forming enhanced biofilms, such as DcprS and Wild type (WT) in MH/deoxycholate (DOC; a bile salt) [19]
Production of a specific surface polysaccharide does not appear to correlate with C. jejuni biofilm formation, unlike in other bacteria
Summary
Campylobacter jejuni is a prevalent food- and waterborne gastrointestinal pathogen. Illness is usually self-limiting, the high incidence of infection, together with the significant subset of cases that go on to manifest as serious autoimmune sequelae (such as Guillain-Barresyndrome), contributes to the significant burden of C. jejuni infection. Preventative strategies that limit C. jejuni exposure and infection may greatly reduce its impact. Mechanisms by which C. jejuni causes disease are relatively enigmatic, suggesting it may use unique strategies compared to more extensively characterized enteric pathogens. In the gastrointestinal tract of commensal or susceptible animals, C. jejuni tolerates insults such as bile salts. C. jejuni is zoonotic, with sporadic cases associated with consumption of undercooked poultry and outbreaks arising from contaminated water, and survives transmission environments characterized by a range of nutrient availabilities, temperatures, oxygen tensions, and osmolarities
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