Editorial: Role of Iron in Bacterial Pathogenesis
Author | Zughaier, Susu M. |
Author | Cornelis, Pierre |
Available date | 2023-09-18T08:50:28Z |
Publication Date | 2018-10-16 |
Publication Name | Frontiers in Cellular and Infection Microbiology |
Identifier | http://dx.doi.org/10.3389/fcimb.2018.00344 |
Citation | Zughaier, S. M., & Cornelis, P. (2018). Role of Iron in bacterial pathogenesis. Frontiers in cellular and infection microbiology, 8, 344. |
ISSN | 2235-2988 |
Abstract | Iron is the fourth-most abundant element on the earth, and it is needed by most organisms, including bacteria. It exists in two oxidation states, Fe2+ and Fe3+, and is involved in many oxido-reduction reactions (Andrews et al., 2013). Ferric iron (Fe3+) is the dominant form in oxygenated environments and has a very low solubility, which presents a problem for microorganisms with an aerobic lifestyle (Andrews et al., 2013). Conversely, in anaerobic environments or in microaerobic conditions at low pH, the soluble ferrous iron (Fe2+) is the most abundant form (Andrews et al., 2003). Bacterial pathogens face a problem because free iron is not available since it is bound to heme or by circulating proteins such as transferrin or lactoferrin (Finkelstein et al., 1983; Cornelissen and Sparling, 1994). Pathogens use different strategies to obtain iron from the host, via the production of extracellular Fe3+-chelating molecules termed siderophores (either their own or produced by other microorganisms), the uptake of heme, and the uptake of Fe2+ (Feo system) (Andrews et al., 2013). A single pathogen can adapt its iron-uptake strategy in response to the type of infection (acute or chronic) and the availability or lack of ferrous iron (Cornelis and Dingemans, 2013). In this issue, several authors present several facets around iron uptake in different bacterial pathogens. Yersinia pestis produces the yersiniabactin siderophore under aerobic conditions and the Feo Fe2+ uptake system under microaerobic conditions (Fetherston et al., 2012). The feo operon of Y. pestis is peculiar since it is repressed by Fe via the Fur repressor only under microaerobic, but not under aerobic conditions, unless the promotor region is truncated. The other facet of the host-pathogen battle for iron is the host response to the bacterial pathogen. As shown, again for Y. pestis, a live vaccine induces an iron nutritional immunity via the production of hemopexin and transferrin iron-binding proteins. |
Language | en |
Publisher | Frontiers Media S.A. |
Subject | host defense against pathogenic bacteria iron depletion iron-regulated genes siderophore virulence factors |
Type | Article |
Volume Number | 8 |
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