Unexpected differential metabolic responses of Campylobacter jejuni to the abundant presence of glutamate and fucose

Abstract

IntroductionCampylobacter jejuni is the leading cause of foodborne bacterial enteritis in humans, and yet little is known in regard to how genetic diversity and metabolic capabilities among isolates affect their metabolic phenotype and pathogenicity.ObjectivesFor instance, the C. jejuni 11168 strain can utilize both l-fucose and l-glutamate as a carbon source, which provides the strain with a competitive advantage in some environments and in this study we set out to assess the metabolic response of C. jejuni 11168 to the presence of l-fucose and l-glutamate in the growth medium.MethodsTo achieve this, untargeted hydrophilic liquid chromatography coupled to mass spectrometry was used to obtain metabolite profiles of supernatant extracts obtained at three different time points up to 24 h.ResultsThis study identified both the depletion and the production and subsequent release of a multitude of expected and unexpected metabolites during the growth of C. jejuni 11168 under three different conditions. A large set of standards allowed identification of a number of metabolites. Further mass spectrometry fragmentation analysis allowed the additional annotation of substrate-specific metabolites. The results show that C. jejuni 11168 upon l-fucose addition indeed produces degradation products of the fucose pathway. Furthermore, methionine was faster depleted from the medium, consistent with previously-observed methionine auxotrophy.ConclusionsMoreover, a multitude of not previously annotated metabolites in C. jejuni were found to be increased specifically upon l-fucose addition. These metabolites may well play a role in the pathogenicity of this C. jejuni strain.Electronic supplementary materialThe online version of this article (10.1007/s11306-018-1438-5) contains supplementary material, which is available to authorized users.

Differences in the Transcriptomic Response of Campylobacter coli and Campylobacter lari to Heat Stress

“…Glutamine is the major nitrogen donor for C. jejuni and C. jejuni 81-176, mutated in the glutamine ABC-Transporter (Cj0469), was more susceptible to heat stress compared to the wild type (Lin et al, 2009). Further, C. jejuni use glutamine as a carbon source (van der Hooft et al, 2018). We determined enhanced gene expression of genes involved in glutamine metabolism for C. coli, like the degenerated ammonium transporter (CCO0599), the glutamine synthetase glnA, the glutamine transporter ATPase glnQ, as well as the adjacent located amino acid transporter permease (CCO1002).…”

Revisiting Campylobacter jejuni Virulence and Fitness Factors: Role in Sensing, Adapting, and Competing

“…The inability to utilize glucose has necessitated C. jejuni to utilize amino acids such as serine, aspartate, glutamate, glutamine, proline and asparagine as carbon and energy sources ( Stahl et al., 2012 ; Hofreuter, 2014 ; Szymanski, 2015 ). Most C. jejuni strains preferentially use serine, aspartate, glutamate, and proline, although certain C. jejuni strains can also utilize asparagine and glutamine ( Thompson and Gaynor, 2008 ; van der Hooft et al., 2018 ). This unique ability to metabolize only a few amino acids allows the bacterium to utilize efficient strategies to include host nutrients into its anabolic processes, to fuel its metabolic pathways and to support its survival and adaptation in hosts with largely commensalism outcome in avian species or pathogenesis in humans.…”

Inhibition of Campylobacter jejuni Biofilm Formation by D-Amino Acids

“…While D-met and D-trp were able to inhibit the biofilm formation of C. jejuni , L-form of those amino acids significantly increased biofilm formation. It is possible that C. jejuni is able to catabolize L-form of those amino acids [ 42 ], which promotes bacterial growth, and consequently formation of the biofilm. This is consistent with the previous report of B. subtilis growth inhibition by D-form of Tyr, Leu, and Trp, and the L-form of those amino acids counteracting this effect [ 24 ].…”