Aims: This study investigated the production and effects of cell-signalling compounds on selected survival and virulence mechanisms of Campylobacter jejuni.

Methods and Results: The production of Autoinducer 1 (AI-1) compounds by Camp. jejuni was investigated in-vitro using a variety of available AI-1 bioassays. We further examined the role of a range of commercially available homoserine
lactones (HSL) and a novel compound (cjA) isolated from Camp. jejuni. The selected attributes included the transformation to a viable but nonculturable (VBNC) state, biofilm formation, interleukin 8 (IL-8) stimulation in
INT-407 cells and virulence gene expression as determined by qRT-PCR. This study is the first to report an HSL or HSL mimic produced by Camp. jejuni. Short chained HSLs and the novel compound cjA prolonged the delay to a VBNC state as well as inhibiting biofilm formation and the majority of HSLs examined and the HSL mimic cjA significantly affected virulence gene expression as well as increasing the production of IL-8 in challenged INT-407 cells.

Conclusions: Despite the lack of a homologous HSL kinase or sensor, Camp. jejuni appears to produce, as well as detect, exogenous signalling molecules and respond accordingly to aid in the survival and virulence capabilities of this micro-organism.

Significance and Impact of the Study: This study suggests that Camp. jejuni is able to detect and utilize as well as possibly produce cell-signalling molecules that enhance both survival and virulence attributes. This possibility opens a new field in the search for Camp. jejuni reduction and elimination strategies.