From food to cell: nutrient exploitation strategies of enteropathogens

Abstract

Upon entering the human gastrointestinal tract, foodborne bacterial enteropathogens encounter, among numerous other stress conditions, nutrient competition with the host organism and the commensal microbiota. The main carbon, nitrogen and energy sources exploited by pathogens during proliferation in, and colonization of, the gut have, however, not been identified completely. In recent years, a huge body of literature has provided evidence that most enteropathogens are equipped with a large set of specific metabolic pathways to overcome nutritional limitations in vivo, thus increasing bacterial fitness during infection. These adaptations include the degradation of myo-inositol, ethanolamine cleaved from phospholipids, fucose derived from mucosal glycoconjugates, 1,2-propanediol as the fermentation product of fucose or rhamnose and several other metabolites not accessible for commensal bacteria or present in competition-free microenvironments. Interestingly, the data reviewed here point to common metabolic strategies of enteric pathogens allowing the exploitation of nutrient sources that not only are present in the gut lumen, the mucosa or epithelial cells, but also are abundant in food. An increased knowledge of the metabolic strategies developed by enteropathogens is therefore a key factor to better control foodborne diseases.

Transcriptomic Analysis of the Adaptation of Listeria monocytogenes to Growth on Vacuum-Packed Cold Smoked Salmon

“…Mapping of these genes to the ethanolamine utilization pathway, constructed based on previous studies for S. enterica (42)(43)(44) and information about the eut operon provided by Staib and Fuchs (44), showed that genes encoding 8 of the 11 key enzymes mapped to the ethanolamine degradation pathway were upregulated (FC, 4.97 to 6.19) (Fig. 2).…”

“…For the galactitol-specific PTS, which includes three components, genes encoding two components (PTS-IIB Gat and PTS-IIC Gat ) were upregulated. For the maltose-specific ABC transporter sys- (42)(43)(44). H7858 protein designations for enzymes involved in these pathways are shown in blue text.…”

“…Furthermore, we identified seven upregulated genes with 1,2-propanediol utilization-related annotations (see Table S4 in the supplemental material) and the GO term "propanediol catabolic process" as overrepresented among upregulated genes (Table 3). We mapped these genes to the 1,2-propanediol utilization pathway, which was constructed based on data from S. enterica (42)(43)(44) and information about the pdu operon provided by Staib and Fuchs (44). This analysis showed that 6 of the 13 genes encoding key enzymes mapped to the 1,2-propanediol degradation pathway (Fig.…”

The Type VI Secretion System Modulates Flagellar Gene Expression and Secretion in Citrobacter freundii and Contributes to Adhesion and Cytotoxicity to Host Cells

“…Ethanolamine is abundant in the intestines of animals and can serve as both a carbon and a nitrogen source. Ethanolamine utilization has been associated with virulence (39,40). Ethanolamine utilization genes have been shown to and their complemented mutants [CF74⌬clpV(pBAD24-clpV), CF74⌬hcp-2(pBAD24-hcp-2), and CF74⌬vgr(pBAD24-vgr)].…”

Genetic Characterization of the Galactitol Utilization Pathway of Salmonella enterica Serovar Typhimurium

“…However, the acquisition of nutrients is a major challenge for S. Typhimurium in the intestine because of the colonization resistance of the commensal microbiota, which confers a highly competitive host environment for substrate availability. To overcome these limitations, enteropathogens have developed specific metabolic capacities that include the utilization of ethanolamine, propanediol, or myo-inositol (7)(8)(9)(10)(11)(12)(13). These catabolic properties are considered critical to virulence; therefore, further characterization of the metabolic profile of S. Typhimurium is of interest.…”