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The ability of Campylobacter (C.) jejuni, the leading cause of food borne bacterial enteritis worldwide, to produce the Quorum sensing molecule autoinducer-2 (AI-2) provides new insights into the mechanisms by which C. jejuni regulates its behavior. The AI-2 mediated Quorum sensing system is widely conserved over both gram-negative and gram-positive bacteria and has been demonstrated to play a critical role in the environmental adaptation of other enteric pathogens such as Escherichia coli and Salmonella spp. Since the discovery of a luxS gene in the C. jejuni genome, which is capable of producing AI-2, various studies have been conducted to explore the function and role of AI-2 in C. jejuni.
AI-2 is a byproduct of the conversion of s-ribosylhomocystein into homocystein in the methionine cycle. Therefore, the C. jejuni luxS mutant phenotypes can either be a result of a changed metabolism or the absence of AI-2. Most studies lack sufficient complementation resulting in not knowing whether phenotypes of luxS mutants should be attributed to a disrupted metabolism or a lack of AI-2. Furthermore, the analysis of phenotypes of the existing C. jejuni luxS mutant could be influenced by differences in strain background, kind of mutation and culture conditions. Additionally, no AI-2 receptor has been found yet for Campylobacter. All this contributes to an extensive discussion about the exact role of AI-2 in C. jejuni. Our work addresses two critical questions regarding AI-2 mediated Quorum sensing of C. jejuni.
First, we provide insight as to why literature about phenotypes of C. jejuni luxS mutants is extremely contradictory. Further, some luxS mutant phenotypes could be partially complemented by AI-2, suggesting that C. jejuni can regulate its behavior by AI-2 dependent Quorum sensing.
Secondly, we demonstrate that AI-2 was not actively taken up by C. jejuni, so further search of AI-2 receptors in C. jejuni should focus on two-component signaling systems or chemoreceptors rather than transporter systems.