ArticleInfection and immunity2004
The nature of extracellular iron influences iron acquisition by Mycobacterium tuberculosis residing within human macrophages.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Dopamine alters macrophage metabolism promoting intracellular Mycobacterium tuberculosis survival.Molecular medicine (Cambridge, Mass.) · 2026Article
- Recent Developments in Drug Delivery for Treatment of Tuberculosis by Targeting Macrophages.Advanced therapeutics · 2022Article
- Host glyceraldehyde-3-phosphate dehydrogenase-mediated iron acquisition is hijacked by intraphagosomal Mycobacterium tuberculosis.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- The Role of Metallic Nanoparticles in Inhibition of Mycobacterium Tuberculosis and Enhances Phagosome Maturation into the Infected Macrophage.Oman medical journal · 2020Review
- Article
- Dual Inhibition ofACS infectious diseases · 2019Article
- Regulation of Three Virulence Strategies of Mycobacterium tuberculosis: A Success Story.International journal of molecular sciences · 2018Review
- Ferritin H Deficiency in Myeloid Compartments Dysregulates Host Energy Metabolism and Increases Susceptibility toFrontiers in immunology · 2018Article
- Elemental Ingredients in the Macrophage Cocktail: Role of ZIP8 in Host Response to Mycobacterium tuberculosis.International journal of molecular sciences · 2017Review
- Gallium nanoparticles facilitate phagosome maturation and inhibit growth of virulent Mycobacterium tuberculosis in macrophages.PloS one · 2017Article
- Article
- Iron Homeostasis in Mycobacterium tuberculosis: Mechanistic Insights into Siderophore-Mediated Iron Uptake.Journal of bacteriology · 2016Review
- Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability.Journal of immunology research · 2016Article
- Prolonged-acting, multi-targeting gallium nanoparticles potently inhibit growth of both HIV and mycobacteria in co-infected human macrophages.Scientific reports · 2015Article
- The exochelins of pathogenic mycobacteria: unique, highly potent, lipid- and water-soluble hexadentate iron chelators with multiple potential therapeutic uses.Antioxidants & redox signaling · 2014Review
- Gallium nitrate is efficacious in murine models of tuberculosis and inhibits key bacterial Fe-dependent enzymes.Antimicrobial agents and chemotherapy · 2013Article
- Iron in intracellular infection: to provide or to deprive?Frontiers in cellular and infection microbiology · 2013Review
- Article
- Gallium disrupts iron uptake by intracellular and extracellular Francisella strains and exhibits therapeutic efficacy in a murine pulmonary infection model.Antimicrobial agents and chemotherapy · 2010Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We have reported that Mycobacterium tuberculosis residing within the phagosomes of human monocyte-derived macrophages (MDM) can acquire Fe from extracellular transferrin (TF) and sources within the MDM. In the lung, Fe is also bound to lactoferrin (LF) and low-molecular-weight chelates. We therefore investigated the ability of intraphagosomal M. tuberculosis to acquire Fe from these sources. M. tuberculosis acquired 30-fold and 3-fold more Fe from LF and citrate, respectively, compared to TF, in spite of similar MDM-associated Fe. M. tuberculosis infection decreased MDM-associated Fe relative to uninfected MDM as follows: TF (38.7%), citrate (21.1%), and LF (15.3%). M. tuberculosis Fe acquisition from extracellular chelates (exogenous source) and from endogenous MDM Fe initially acquired from the three chelates (endogenous source) was compared. M. tuberculosis Fe acquisition was similar from exogenous and endogenous sources supplied as Fe-TF. In contrast, there was much greater intracellular M. tuberculosis Fe uptake from LF and citrate from the exogenous than endogenous source. Gamma interferon (IFN-gamma) reduced MDM Fe uptake from each chelate by approximately 50% and augmented the M. tuberculosis-induced decrease in MDM Fe uptake from exogenous TF, but not from LF or citrate. IFN-gamma minimally decreased intracellular M. tuberculosis Fe acquisition from exogenous Fe-TF but significantly increased Fe uptake from LF and citrate. Intraphagosomal M. tuberculosis Fe acquisition from both exogenous and endogenous MDM sources, and the effect of IFN-gamma on this process, is influenced by the nature of the extracellular Fe chelate. M. tuberculosis has developed efficient mechanisms of acquiring Fe from a variety of Fe chelates that it likely encounters within the human lung.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.