Plasmid-Encoded Iron Uptake Systems

Abstract

Plasmids confer genetic information that benefits the bacterial cells containing them. In pathogenic bacteria, plasmids often harbor virulence determinants that enhance the pathogenicity of the bacterium. The ability to acquire iron in environments where it is limited, for instance the eukaryotic host, is a critical factor for bacterial growth. To acquire iron, bacteria have evolved specific iron uptake mechanisms. These systems are often chromosomally encoded, while those that are plasmid-encoded are rare. Two main plasmid types, ColV and pJM1, have been shown to harbor determinants that increase virulence by providing the cell with essential iron for growth. It is clear that these two plasmid groups evolved independently from each other since they do not share similarities either in the plasmid backbones or in the iron uptake systems they harbor. The siderophores aerobactin and salmochelin that are found on ColV plasmids fall in the hydroxamate and catechol group, respectively, whereas both functional groups are present in the anguibactin siderophore, the only iron uptake system found on pJM1-type plasmids. Besides siderophore-mediated iron uptake, ColV plasmids carry additional genes involved in iron metabolism. These systems include ABC transporters, hemolysins, and a hemoglobin protease. ColV-and pJM1-like plasmids have been shown to confer virulence to their bacterial host, and this trait can be completely ascribed to their encoded iron uptake systems.

Horizontally acquired papGII-containing pathogenicity islands underlie the emergence of invasive uropathogenic Escherichia coli lineages

“…Iron acquisition systems are regarded as critical virulence factors of UPEC 36 . Of the 22 presumably partially redundant iron uptake systems described for E. coli [37][38][39] , the average number of such systems per isolate was significantly higher among invasive UPEC isolates (15.6) than among cystitis isolates (14.3), ABU isolates (14.0), or fecal isolates (12.9) (Supplementary Table 9). papGII+ isolates carried, on average, 16.3 iron uptake systems (vs. 13.5 among papGII-negative isolates, P < 0.001).…”

Plasmid dispersal and recombination across human gut microbiomes is neutral, but overpowered by inflammatory diseases

“…Among individuals with IBD, we identified 830 segments that were significantly shared across continents, with 525 carrying annotated functions. Notably, the "ABC transporters" pathway was enriched in cross-continental segments in IBD samples, including proteins of the SitABCD system involved in manganese/iron transport systems, previously identified on plasmids 37 . Iron deficiency anemia is a common complication in IBD, where iron leaking from the intestinal environment is sequestered mainly by pathogenic bacteria in the gut, transforming commensal gut microbes into pathobionts and inducing inflammation 38 .…”