Iron in intracellular infection: to provide or to deprive?
Identifieur interne : 000221 ( Main/Exploration ); précédent : 000220; suivant : 000222Iron in intracellular infection: to provide or to deprive?
Auteurs : Sandro Silva-Gomes [Portugal] ; Sílvia Vale-Costa [Portugal] ; Rui Appelberg [Portugal] ; Maria S. Gomes [Portugal]Source :
- Frontiers in Cellular and Infection Microbiology [ 2235-2988 ] ; 2013.
Abstract
Due to their chemical versatility, transition metals were incorporated as cofactors for several basic metabolic pathways in living organisms. This same characteristic makes them potentially harmful, since they can be engaged in deleterious reactions like Fenton chemistry. As such, organisms have evolved highly specialized mechanisms to supply their own metal needs while keeping their toxic potential in check. This dual character comes into play in host-pathogen interactions, given that the host can either deprive the pathogen of these key nutrients or exploit them to induce toxicity toward the invading agent. Iron stands as the prototypic example of how a metal can be used to limit the growth of pathogens by nutrient deprivation, a mechanism widely studied in
Url:
DOI: 10.3389/fcimb.2013.00096
PubMed: 24367768
PubMed Central: 3856365
Affiliations:
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Gomes</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Infection and Immunity Unit, Instituto de Biologia Molecular e Celular, Universidade do Porto</institution><country>Porto, Portugal</country></nlm:aff><country xml:lang="fr">Portugal</country><wicri:regionArea></wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Molecular Biology, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto</institution><country>Porto, Portugal</country></nlm:aff><country xml:lang="fr">Portugal</country><wicri:regionArea></wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Cellular and Infection Microbiology</title><idno type="eISSN">2235-2988</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Due to their chemical versatility, transition metals were incorporated as cofactors for several basic metabolic pathways in living organisms. This same characteristic makes them potentially harmful, since they can be engaged in deleterious reactions like Fenton chemistry. As such, organisms have evolved highly specialized mechanisms to supply their own metal needs while keeping their toxic potential in check. This dual character comes into play in host-pathogen interactions, given that the host can either deprive the pathogen of these key nutrients or exploit them to induce toxicity toward the invading agent. Iron stands as the prototypic example of how a metal can be used to limit the growth of pathogens by nutrient deprivation, a mechanism widely studied in <italic>Mycobacterium</italic> infections. However, the host can also take advantage of iron-induced toxicity to control pathogen proliferation, as observed in infections caused by <italic>Leishmania</italic>. Whether we may harness either of the two pathways for therapeutical purposes is still ill-defined. In this review, we discuss how modulation of the host iron availability impacts the course of infections, focusing on those caused by two relevant intracellular pathogens, <italic>Mycobacterium</italic> and <italic>Leishmania</italic>.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ait Oudhia, K" uniqKey="Ait Oudhia K">K. Ait-Oudhia</name></author><author><name sortKey="Gazanion, E" uniqKey="Gazanion E">E. Gazanion</name></author><author><name sortKey="Vergnes, B" uniqKey="Vergnes B">B. Vergnes</name></author><author><name sortKey="Oury, B" uniqKey="Oury B">B. Oury</name></author><author><name sortKey="Sereno, D" uniqKey="Sereno D">D. Sereno</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Altet, L" uniqKey="Altet L">L. Altet</name></author><author><name sortKey="Francino, O" uniqKey="Francino O">O. Francino</name></author><author><name sortKey="Solano Gallego, L" uniqKey="Solano Gallego L">L. 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Jiang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zwilling, B S" uniqKey="Zwilling B">B. S. Zwilling</name></author><author><name sortKey="Kuhn, D E" uniqKey="Kuhn D">D. E. Kuhn</name></author><author><name sortKey="Wikoff, L" uniqKey="Wikoff L">L. Wikoff</name></author><author><name sortKey="Brown, D" uniqKey="Brown D">D. Brown</name></author><author><name sortKey="Lafuse, W" uniqKey="Lafuse W">W. Lafuse</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Portugal</li></country></list><tree><country name="Portugal"><noRegion><name sortKey="Silva Gomes, Sandro" sort="Silva Gomes, Sandro" uniqKey="Silva Gomes S" first="Sandro" last="Silva-Gomes">Sandro Silva-Gomes</name></noRegion><name sortKey="Appelberg, Rui" sort="Appelberg, Rui" uniqKey="Appelberg R" first="Rui" last="Appelberg">Rui Appelberg</name><name sortKey="Appelberg, Rui" sort="Appelberg, Rui" uniqKey="Appelberg R" first="Rui" last="Appelberg">Rui Appelberg</name><name sortKey="Gomes, Maria S" sort="Gomes, Maria S" uniqKey="Gomes M" first="Maria S." last="Gomes">Maria S. Gomes</name><name sortKey="Gomes, Maria S" sort="Gomes, Maria S" uniqKey="Gomes M" first="Maria S." last="Gomes">Maria S. Gomes</name><name sortKey="Silva Gomes, Sandro" sort="Silva Gomes, Sandro" uniqKey="Silva Gomes S" first="Sandro" last="Silva-Gomes">Sandro Silva-Gomes</name><name sortKey="Vale Costa, Silvia" sort="Vale Costa, Silvia" uniqKey="Vale Costa S" first="Sílvia" last="Vale-Costa">Sílvia Vale-Costa</name><name sortKey="Vale Costa, Silvia" sort="Vale Costa, Silvia" uniqKey="Vale Costa S" first="Sílvia" last="Vale-Costa">Sílvia Vale-Costa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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