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Posted by peklebba on 30 Nov 2012 at 17:24 GMT
As a result of iron's central role in biochemistry, bacteria and animals engage in a constant microbiological battle to obtain the metal. Iron is a valuable commodity in biochemistry, and its acquisition in the host environment was reported as a determinant of bacterial virulence. Nevertheless, this concept remains controversial as a result of conflicting data, and little is known about what forms of iron are available and utilized by enteric bacteria during colonization of the host gut. Previous experiments studied mouse infection by "Salmonella typhimurium" or "Escherichia coli" strains that were impaired in the acquisition of the native Gram-negative bacterial siderophore, enterobactin, and concluded that this attribute was inconsequential to colonization. We reassessed these conclusions with genetically engineered "E. coli" strains that systematically separated and evaluated the importance of enterobactin synthesis and ferric enterobactin uptake. The findings explain and resolve the conflicting data, eliminating any doubt about the importance of catecholate siderophores in bacterial colonization of animals: the complete inability to transport ferric enterobactin created an immense defect in bacterial survival in the mouse gut. It was also telling that in the presence of a competing strain that was competent for enterobactin synthesis but deficient in ferric enterobactin transport (a condition that resulted in enterobactin hyperexcretion), wild-type "E. coli" proliferated to 100-fold higher than normal levels in mice (Fig. 3, center). These data demonstrate the facilitation of Gram-negative bacterial colonization by siderophore-mediated iron acquisition in the gut.