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References2026-06-27
Mycobacterium tuberculosis majorMicrobe page published: biology, metallome and virulence, host nutritional immunity, triangle-tested interventions, and the full research feed of studies mentioning the organism.
Did you know?
Mycobacterium tuberculosis is an obligate aerobe held dormant by the granuloma's low oxygen, so raising tissue oxygen is the wrong lever, the opposite of anaerobe-driven infections.
Mycobacterium tuberculosis (M. tb)
Mycobacterium tuberculosis (Mtb) is the obligate-aerobic, acid-fast bacillus that causes tuberculosis, an intracellular macrophage pathogen and iron pirate that survives phagosomal copper/zinc intoxication and granuloma hypoxia.
Page Snapshot
Microbiome-targeted interventions (MBTIs) are validated using a dual-evidence logical framework. First, the intervention must realign the condition’s microbiome signature by increasing beneficial taxa that are consistently depleted and reducing pathogenic taxa that are consistently enriched. Second, the intervention must demonstrate measurable clinical benefit. Concordance of these effects in the same context validates the intervention as an MBTI and supports the clinical relevance of the microbiome signature.
Karen Pendergrass
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreOverview
Mycobacterium tuberculosis (Mtb) is the obligate-aerobic, acid-fast bacillus that causes tuberculosis (TB) and remains one of the world's deadliest single pathogens.[1] Spread by respiratory aerosols, it is an intracellular parasite of the macrophage: after phagocytosis it arrests phagosome maturation and persists in the very cell meant to kill it. Most infected hosts contain the bacillus in a clinically silent latent state, while roughly 5–10% progress to active disease, an outcome set at the host–pathogen interface rather than by the organism alone.
What makes Mtb distinctive on this database is how it fights for metals and oxygen. It is, above all, an iron pirate: it strips host iron using the siderophores mycobactin and carboxymycobactin, imported through the IrtAB transporter under IdeR control,[2][3][4] while the host withholds iron through hepcidin, lactoferrin, transferrin, and siderocalin.[5] Because iron feeds the bacillus, iron loading and high ferritin track with worse outcomes[6][7], the low serum iron of active TB is usually host defense, not a deficiency to correct.
Biology and lifestyle
Mtb is a slow-growing obligate aerobe. Inside the granuloma's caseous core it meets falling oxygen, and because it cannot ferment, hypoxia does not kill it, it forces a non-replicating dormancy through the DosR regulon, the molecular basis of latency and of decades-long persistence.[8][9] Reoxygenation permits regrowth, which is why raising tissue oxygen is the wrong lever for TB, the opposite of anaerobe-dominated infections. The bacillus is, however, vulnerable to host redox chemistry: glutathione and its precursor N-acetylcysteine have direct anti-mycobacterial activity within the granuloma.[10]
Metallome
How M. tuberculosis acquires, uses, and detoxifies each metal ion at the host–pathogen interface. The macrophage attacks on two fronts at once, iron and manganese withholding, copper and zinc intoxication[11], and Mtb carries a dedicated transporter for each. Metals with no characterized Mtb biology (mercury, tin, aluminum, chromium) are omitted.
| Metal / Ion | Key Features in M. tuberculosis |
|---|---|
| Iron (Fe) | The master nutrient. Strips host iron with the siderophores mycobactin and carboxymycobactin, imported through the IrtAB transporter under IdeR control.[2][3][4] |
| Copper (Cu) | Survives macrophage copper poisoning via the efflux ATPase CtpV, the sensor CsoR, and the channel MctB, all virulence-essential.[12] |
| Zinc (Zn) | Counters host zinc intoxication of the phagosome with the P-type ATPase CtpC.[13] |
| Manganese (Mn) | Withheld by neutrophil calprotectin (Mn/Zn) and the phagosomal transporter NRAMP1/SLC11A1, whose variants alter susceptibility.[14][15] |
| Cadmium (Cd) | The ArsR-SmtB sensor CmtR (Rv1994c) derepresses the P-type ATPase CtpG to efflux cadmium.[16] |
| Lead (Pb) | The same CmtR/CtpG operon also effluxes lead, a shared P-ATPase route detoxifying both Cd and Pb.[16] |
| Arsenic (As) | Detoxified by a distinctive fused Acr3–ArsC polypeptide (a single 498-amino-acid protein) that performs both arsenate reduction and arsenite efflux.[17] |
| Nickel (Ni) / Cobalt (Co) | Nickel is a pathogen virulence cofactor, the catalytic metal of ureases and [NiFe] hydrogenases, opposed by host calprotectin sequestration.[18] M. tuberculosis runs a nickel-dependent urease (the ureABCFGD locus) that supports nitrogen acquisition and blunts phagosomal acidification,[19] and balances cytoplasmic Ni/Co with the ArsR-SmtB sensor NmtR, which derepresses a P-type ATPase (CtpJ) to export the metals.[20] |
Virulence Factors
The factors that let M. tuberculosis enter, subvert, and persist inside the macrophage, several of which (the copper/zinc-resistance ATPases, the iron siderophores) are the same metal-handling systems above, tying the metallome directly to virulence.
| Virulence Factors | Description and Role |
|---|---|
| ESX-1 secretion system (ESAT-6/CFP-10) | Type VII secretion system; EsxA ruptures the phagosomal membrane, giving Mtb access to the host cytosol.[21] |
| PDIM (phthiocerol dimycocerosates) | Surface lipids that mask pathogen-associated molecular patterns and cooperate with ESX-1 in phagosomal membrane damage and escape.[21] |
| Cord factor (trehalose-6,6-dimycolate) | Binds the Mincle receptor to drive cytokine production and granuloma formation.[21] |
| ManLAM (mannosylated lipoarabinomannan) | Arrests phagosome maturation, protecting Mtb from phagolysosomal degradation.[21] |
| Mycobactin / carboxymycobactin siderophores | Pirate host iron under nutritional-immunity iron restriction, the central nutritional–virulence link.[2][3] |
| Cu/Zn-resistance ATPases (CtpV, MctB, CtpC) | Pump out phagosomal copper and zinc, surviving the macrophage's metal-intoxication assault, loss of copper resistance is de-virulencing.[12][13] |
| PknG and SapM | Secreted effectors that block phagosome–lysosome fusion, sustaining intracellular survival.[21] |
How the host fights it
Beyond the phagosomal metal battle, the host deploys systemic nutritional immunity: IL-6 drives hepcidin, degrading ferroportin to produce the hypoferremia and anemia of inflammation that starve the bacillus;[22] lactoferrin reinforces iron-withholding and lowers mycobacterial burden in iron-overloaded hosts;[23] and siderocalin intercepts Mtb's carboxymycobactin directly.[5] At the mucosa, the airway and gut microbiome shape this defense, active disease shows a collapse of airway diversity with enrichment of oral-origin anaerobes,[24][25][26] and gut-lung-axis dysbiosis with loss of short-chain-fatty-acid producers may blunt protective immunity[27][28] (associative, and heavily antibiotic-confounded).
Interventions
Our validation method evaluates each candidate against M. tuberculosis with the Triangle Test, then classifies it as Validated, Promising Candidate, or Validation In Progress. All of the below are host-directed adjuncts to standard multidrug chemotherapy (isoniazid, rifampicin, pyrazinamide, ethambutol, or the appropriate drug-resistant regimen); none replaces it.
| Intervention | Classification | Status |
|---|---|---|
| N-acetylcysteine (NAC) | Supplement | Promising Candidate |
| Vitamin D | Supplement | Promising Candidate |
| L-arginine / nitric oxide | Supplement | Promising Candidate |
| Lactoferrin | Supplement | Validation In Progress |
| Iron restriction / chelation | Diet / Pharmaceutical | Validation In Progress |
How do these interventions act on M. tuberculosis?
| Intervention | Classification | Notes |
| N-acetylcysteine (NAC) | Supplement | Restores glutathione and is directly anti-mycobacterial;[29] a 140-patient RCT confirmed glutathione repletion and better lung-function recovery but no faster culture conversion.[30] |
| Vitamin D | Supplement | Induces cathelicidin (LL-37) and autophagy against intracellular Mtb;[31] an IPD meta-analysis found no overall culture-conversion benefit but marked acceleration in multidrug-resistant TB.[32] |
| L-arginine | Supplement | Substrate for macrophage nitric oxide; one RCT positive in HIV-negative patients.[33] |
| Lactoferrin | Supplement | Reinforces iron-withholding and shifts immunity toward Th1; reduces Mtb burden in iron-overloaded models.[34][23] |
| Metformin | Drug Repurposing | AMPK-driven autophagy; observational mortality benefit in diabetics with TB.[35] |
| Statins | Drug Repurposing | Mtb consumes host cholesterol;[36] statins shorten treatment in mice.[37] |
What should be avoided (STOP)?
Routine iron supplementation during active TB: the low serum iron is hepcidin-driven sequestration (host defense), not deficiency, and exogenous iron can feed Mtb's siderophore machinery while iron loading independently worsens outcomes.[38][39] Reserve iron for documented true iron-deficiency anemia, cautiously.
Frequently Asked Questions
What is Mycobacterium tuberculosis (M. tb)?
Quick answer: Mycobacterium tuberculosis (Mtb) is the obligate-aerobic, acid-fast bacillus that causes tuberculosis (TB) and remains one of the world's deadliest single pathogens. [1] Spread by respiratory aerosols, it is an intracellular parasite of the macrophage: after phagocytosis it arrests phagosome maturation and persists in the very cell meant to kill it. Most infected hosts contain the bacillus in a clinically silent latent state, while roughly 5–10% progress to active disease—an outcome set at the host–pathogen interface rather than by the organism alone.
What helps treat Mycobacterium tuberculosis (M. tb)?
Quick answer: Our validation method evaluates each candidate against M. tuberculosis with the Triangle Test, then classifies it as Validated, Promising Candidate, or Validation In Progress. All of the below are host-directed adjuncts to standard multidrug chemotherapy (isoniazid, rifampicin, pyrazinamide, ethambutol, or the appropriate drug-resistant regimen); none replaces it.
Research Feed
Dissecting the effect of single- and co-infection of TB and COVID-19 pathogens on the sputum microbiome
2026
/
Research Feed
A four-group sputum microbiome study in India found that tuberculosis and COVID-19 co-infection reshaped airway bacterial composition and upregulated surfactant-lipid metabolic pathways relative to TB alone, with shifts that tracked toward adverse TB outcomes.
A four-group sputum microbiome study in India found that tuberculosis and COVID-19 co-infection reshaped airway bacterial composition and upregulated surfactant-lipid metabolic pathways relative to TB alone, with shifts that tracked toward adverse TB outcomes.
Interplay between gut microbiota and the master iron regulator, hepcidin, in the pathogenesis of liver fibrosis
2026
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Research Feed
This minireview synthesizes how gut dysbiosis and hepcidin-driven iron mismanagement reinforce hepatic inflammation and stellate-cell activation in fibrosis, highlighting SCFAs, LPS/TLR4 signaling, and microbiota effects on intestinal iron transport as actionable pathways.
This minireview synthesizes how gut dysbiosis and hepcidin-driven iron mismanagement reinforce hepatic inflammation and stellate-cell activation in fibrosis, highlighting SCFAs, LPS/TLR4 signaling, and microbiota effects on intestinal iron transport as actionable pathways.
Additive Effects of Glutathione in Improving Antibiotic Efficacy in HIV–M.tb Co-Infection in the Central Nervous System: A Systematic Review
2025
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Research Feed
This review explores the potential of glutathione supplementation in improving antibiotic efficacy and immune responses in HIV-M.tb co-infection, particularly in CNS cases.
This review explores the potential of glutathione supplementation in improving antibiotic efficacy and immune responses in HIV-M.tb co-infection, particularly in CNS cases.
Glutathione and Adaptive Immune Responses against Mycobacterium tuberculosis Infection in Healthy and HIV Infected Individuals
2025
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Research Feed
This study examines how glutathione influences T cell function in HIV and tuberculosis co-infection. It reveals that restoring GSH levels enhances cytokine production and controls M. tb growth, suggesting therapeutic potential for GSH-based interventions in HIV-infected individuals.
This study examines how glutathione influences T cell function in HIV and tuberculosis co-infection. It reveals that restoring GSH levels enhances cytokine production and controls M. tb growth, suggesting therapeutic potential for GSH-based interventions in HIV-infected individuals.
The Role of Glutathione in the Management of Cell-Mediated Immune Responses in Individuals with HIV
2025
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Research Feed
This review shows that glutathione depletion drives immune dysfunction in HIV by disrupting T-cell balance, gut immunity, and pathogen control, while supplementation restores immune signaling and reduces inflammation.
This review shows that glutathione depletion drives immune dysfunction in HIV by disrupting T-cell balance, gut immunity, and pathogen control, while supplementation restores immune signaling and reduces inflammation.
Glutathione Modulates Efficacious Changes in the Immune Response against Tuberculosis
2025
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Research Feed
This review shows that glutathione restores immune balance, limits oxidative stress, and improves host defense against Mycobacterium tuberculosis infection.
This review shows that glutathione restores immune balance, limits oxidative stress, and improves host defense against Mycobacterium tuberculosis infection.
Glutathione Depletion Exacerbates Hepatic Mycobacterium tuberculosis Infection
2025
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Research Feed
This study shows that glutathione depletion in hepatic tuberculosis increases oxidative stress, disrupts immune signaling, damages granulomas, and promotes Mycobacterium tuberculosis survival.
This study shows that glutathione depletion in hepatic tuberculosis increases oxidative stress, disrupts immune signaling, damages granulomas, and promotes Mycobacterium tuberculosis survival.
Transition metals and virulence in bacteria
2025
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Research Feed
What was reviewed? This review article examines how transition metals shape bacterial virulence through three interconnected processes: acquisition, limitation, and intoxication. It emphasizes the evolutionary “arms race” between microbial strategies for metal uptake and host mechanisms for nutritional immunity. The review highlights how iron, zinc, and manganese, critical cofactors for bacterial metabolism, are sequestered, restricted, or weaponized […]
What was reviewed? This review article examines how transition metals shape bacterial virulence through three interconnected processes: acquisition, limitation, and intoxication. It emphasizes the evolutionary “arms race” between microbial strategies for metal uptake and host mechanisms for nutritional immunity. The review highlights how iron, zinc, and manganese, critical cofactors for bacterial metabolism, are sequestered, restricted, or weaponized […]
Gallium as novel Antimicrobial Agents: Innovations in Combating Drug-Resistant Pathogens
2025
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Research Feed
This review highlights gallium’s role as an iron mimic disrupting bacterial iron metabolism, effective against multidrug-resistant pathogens. Innovations in gallium delivery, including nanomaterials and synergistic therapies with antibiotics, address bioavailability challenges and enhance its antimicrobial potency.
This review highlights gallium’s role as an iron mimic disrupting bacterial iron metabolism, effective against multidrug-resistant pathogens. Innovations in gallium delivery, including nanomaterials and synergistic therapies with antibiotics, address bioavailability challenges and enhance its antimicrobial potency.
Altered Actinobacteria and Firmicutes Phylum Associated Epitopes in Patients With Parkinson’s Disease
2025
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Research Feed
Altered Actinobacteria and Firmicutes gut microbiota, and their associated epitopes, are strongly linked to inflammation and metabolic changes in Parkinson’s disease, suggesting novel mechanisms underlying PD pathogenesis and offering potential new biomarkers for diagnosis and intervention.
Altered Actinobacteria and Firmicutes gut microbiota, and their associated epitopes, are strongly linked to inflammation and metabolic changes in Parkinson’s disease, suggesting novel mechanisms underlying PD pathogenesis and offering potential new biomarkers for diagnosis and intervention.
Disulfiram and Copper Ions Kill Mycobacterium tuberculosis in a Synergistic Manner
2025
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Research Feed
This study shows that disulfiram, in combination with copper ions, significantly enhances the bactericidal effects against M. tuberculosis, especially against drug-resistant strains. The copper-dependent activity of disulfiram offers a potential new therapeutic approach for tuberculosis.
This study shows that disulfiram, in combination with copper ions, significantly enhances the bactericidal effects against M. tuberculosis, especially against drug-resistant strains. The copper-dependent activity of disulfiram offers a potential new therapeutic approach for tuberculosis.
The Promise of Copper Ionophores as Antimicrobials
2025
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Research Feed
The promise of copper ionophores as antimicrobials rests on raising intracellular copper to disable core enzymes, restore antibiotic activity, and boost host killing, with clear microbial markers to track response.
The promise of copper ionophores as antimicrobials rests on raising intracellular copper to disable core enzymes, restore antibiotic activity, and boost host killing, with clear microbial markers to track response.
Zinc in Human Health and Infectious Diseases
2025
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Research Feed
This review maps zinc in human health and infectious diseases, linking host zinc control to pathogen survival, clinical trial signals, and simple gene and protein markers that explain microbiome shifts under zinc pressure.
This review maps zinc in human health and infectious diseases, linking host zinc control to pathogen survival, clinical trial signals, and simple gene and protein markers that explain microbiome shifts under zinc pressure.
Mycobacterium tuberculosis and Copper: A Newly Appreciated Defense against an Old Foe?
2025
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Research Feed
Mycobacterium tuberculosis and copper shows copper rises at infection sites, while bacterial systems (MctB, CsoR–CtpV, RicR–MymT/MmcO) defend against toxicity; these markers inform clinical risk and target discovery.
Mycobacterium tuberculosis and copper shows copper rises at infection sites, while bacterial systems (MctB, CsoR–CtpV, RicR–MymT/MmcO) defend against toxicity; these markers inform clinical risk and target discovery.
Copper resistance is essential for virulence of Mycobacterium tuberculosis
2025
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Research Feed
Copper resistance is essential for virulence of Mycobacterium tuberculosis; MctB prevents copper build-up, and loss of MctB cripples survival in copper-rich granulomas, defining actionable microbial and host signatures.
Copper resistance is essential for virulence of Mycobacterium tuberculosis; MctB prevents copper build-up, and loss of MctB cripples survival in copper-rich granulomas, defining actionable microbial and host signatures.
CtpB Facilitates Mycobacterium tuberculosis Growth in Copper-Limited Niches
2025
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Research Feed
CtpB tailors Mycobacterium tuberculosis growth to copper-limited niches, boosts fitness in adipocytes, and raises copper stress risk during phagosomal surges, yielding a clear gene–niche signature for clinical use.
CtpB tailors Mycobacterium tuberculosis growth to copper-limited niches, boosts fitness in adipocytes, and raises copper stress risk during phagosomal surges, yielding a clear gene–niche signature for clinical use.
The interplay between copper metabolism and microbes: In perspective of host copper-dependent ATPases ATP7A/B
2025
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Research Feed
This review highlights the complex relationship between copper metabolism and microbial infections. It focuses on the role of copper transporters ATP7A/B in regulating copper homeostasis and how microbes manipulate these mechanisms to survive in the host.
This review highlights the complex relationship between copper metabolism and microbial infections. It focuses on the role of copper transporters ATP7A/B in regulating copper homeostasis and how microbes manipulate these mechanisms to survive in the host.
The Role of Copper and Zinc Toxicity in Innate Immune Defense against Bacterial Pathogens
2025
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Research Feed
Copper and zinc toxicity in innate immunity drives early control of bacterial pathogens and shapes mucosal niches. The review links host metal routing and microbial export genes to killing, virulence, and microbiome shifts.
Copper and zinc toxicity in innate immunity drives early control of bacterial pathogens and shapes mucosal niches. The review links host metal routing and microbial export genes to killing, virulence, and microbiome shifts.
Copper at the Front Line of the Host-Pathogen Battle
2025
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Research Feed
This review explores the critical role of copper in microbial pathogenesis, focusing on how the host uses it as an antimicrobial weapon and how pathogens resist Cu toxicity. It suggests potential therapeutic avenues targeting Cu resistance mechanisms.
This review explores the critical role of copper in microbial pathogenesis, focusing on how the host uses it as an antimicrobial weapon and how pathogens resist Cu toxicity. It suggests potential therapeutic avenues targeting Cu resistance mechanisms.
Copper in microbial pathogenesis: Meddling with the metal
2025
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Research Feed
This review explores copper’s role in microbial pathogenesis, highlighting its use by hosts as an antimicrobial weapon and the resistance mechanisms developed by pathogens. It discusses copper’s involvement in immune defense and fungal virulence, offering insights into potential therapeutic strategies.
This review explores copper’s role in microbial pathogenesis, highlighting its use by hosts as an antimicrobial weapon and the resistance mechanisms developed by pathogens. It discusses copper’s involvement in immune defense and fungal virulence, offering insights into potential therapeutic strategies.
Siderophore Biosynthesis Inhibitors: A Novel Strategy Against Microbial Virulence and Resistance
2025
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Research Feed
This review outlines current strategies targeting siderophore biosynthesis as a therapeutic approach to microbial infections, emphasizing enzyme-specific inhibitors, nanoparticle delivery, and CRISPR-based interventions to impair iron acquisition and reduce virulence.
This review outlines current strategies targeting siderophore biosynthesis as a therapeutic approach to microbial infections, emphasizing enzyme-specific inhibitors, nanoparticle delivery, and CRISPR-based interventions to impair iron acquisition and reduce virulence.
Recent Advances in Siderophore Biosynthesis Pathways: Implications for Microbial Virulence and Therapeutics
2025
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Research Feed
This review details recent enzymatic and structural insights into NRPS-dependent and NRPS-independent siderophore biosynthesis, emphasizing implications for antimicrobial development and microbiome-targeted therapies.
This review details recent enzymatic and structural insights into NRPS-dependent and NRPS-independent siderophore biosynthesis, emphasizing implications for antimicrobial development and microbiome-targeted therapies.
Lipocalin 2 and the iroA gene cluster in host iron defense and evasion
2025
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Research Feed
Lipocalin 2 sequesters enterobactin to starve bacteria of iron, while the iroA cluster glucosylates enterobactin into salmochelins that evade capture, sustaining virulence. Targeting iroA may restore host iron withholding without disrupting commensals.
Lipocalin 2 sequesters enterobactin to starve bacteria of iron, while the iroA cluster glucosylates enterobactin into salmochelins that evade capture, sustaining virulence. Targeting iroA may restore host iron withholding without disrupting commensals.
Role of Iron in Bacterial Pathogenesis: Clinical Takeaways from an Editorial
2025
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Research Feed
What was reviewed? This editorial synthesizes evidence on the role of iron in bacterial pathogenesis, emphasizing how iron scarcity and host nutritional immunity shape virulence, metabolic strategy, and antibiotic tolerance across diverse pathogens. Mechanisms covered include siderophore production and piracy, heme acquisition, ferrous iron uptake via Feo, and regulatory circuitry such as Fur and the […]
What was reviewed? This editorial synthesizes evidence on the role of iron in bacterial pathogenesis, emphasizing how iron scarcity and host nutritional immunity shape virulence, metabolic strategy, and antibiotic tolerance across diverse pathogens. Mechanisms covered include siderophore production and piracy, heme acquisition, ferrous iron uptake via Feo, and regulatory circuitry such as Fur and the […]
Nutritional Immunity and Metallomic Signatures: Metal Competition at the Host–Pathogen Interface
2025
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Research Feed
This review details how nutritional immunity shapes host–pathogen interactions through metal sequestration and intoxication, highlights key microbial metal acquisition systems, and discusses their implications for microbiome signatures and the development of novel antimicrobial therapies.
This review details how nutritional immunity shapes host–pathogen interactions through metal sequestration and intoxication, highlights key microbial metal acquisition systems, and discusses their implications for microbiome signatures and the development of novel antimicrobial therapies.
Copper in microbial pathogenesis: meddling with the metal
2025
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Research Feed
What was studied? The study investigated the role of copper in microbial pathogenesis. Specifically, it examined how copper serves as both a necessary nutrient for microbial organisms and a microbial weapon used by hosts against pathogens. The research explored copper’s dual roles, its involvement in various microbial resistance mechanisms, and its interaction with the host’s […]
What was studied? The study investigated the role of copper in microbial pathogenesis. Specifically, it examined how copper serves as both a necessary nutrient for microbial organisms and a microbial weapon used by hosts against pathogens. The research explored copper’s dual roles, its involvement in various microbial resistance mechanisms, and its interaction with the host’s […]
Update History
References
- Global Tuberculosis Report 2024 World Health Organization. (WHO, 2024)
- Iron Homeostasis in Mycobacterium tuberculosis: siderophore-mediated iron uptake. Sritharan M. (J Bacteriol. 2016)
- Identification of an ABC transporter required for iron acquisition and virulence in M. tuberculosis (IrtAB). Rodriguez GM, Smith I. (J Bacteriol. 2006)
- IdeR controls iron acquisition, storage and survival in macrophages. Gold B, Rodriguez GM, et al. (Mol Microbiol. 2001)
- Siderocalin (Lcn2) binds carboxymycobactins, defending against mycobacterial infection. Holmes MA, et al. (Structure. 2005)
- Tuberculosis and iron overload in Africa: a review. Gangaidzo IT, Gordeuk VR. (Cent Afr J Med. 1995)
- Iron Status Predicts Treatment Failure and Mortality in Tuberculosis Patients. Isanaka S, et al. (PLoS One. 2012)
- The M. tuberculosis DosR regulon and recovery from nonrespiring dormancy. Leistikow RL, et al. (J Bacteriol. 2010)
- M. tuberculosis relies on trace oxygen to survive hypoxic environments (obligate aerobe). Kalia NP, et al. (Cell Rep. 2023)
- Synergistic effects of NAC and first-line antibiotics in the granulomatous response to Mtb. Teskey G, et al. (Front Immunol. 2018)
- Zinc and copper toxicity in host defense against pathogens: M. tuberculosis as a model. Neyrolles O, Mintz E, Catty P. (Front Cell Infect Microbiol. 2013)
- Copper resistance is essential for virulence of Mycobacterium tuberculosis. Wolschendorf F, et al. (PNAS. 2011)
- Mycobacterial P1-type ATPases mediate resistance to zinc poisoning in human macrophages. Botella H, et al. (Cell Host Microbe. 2011)
- Molecular basis for manganese sequestration by calprotectin. Damo SM, et al. (PNAS. 2013)
- SLC11A1 (NRAMP1) polymorphisms and tuberculosis susceptibility: meta-analysis. Li X, et al. (PLoS One. 2011)
- Metallobiology of Tuberculosis. Rodriguez GM, Neyrolles O. (Microbiol Spectr. 2014)
- Distribution of Arsenic Resistance Genes in Prokaryotes. Ben Fekih I, et al. (Front Microbiol. 2018)
- Role of Nickel in Microbial Pathogenesis. Maier RJ, Benoit SL. (Inorganics. 2019;7(7):80)
- Purification, characterization, and genetic analysis of Mycobacterium tuberculosis urease, a potentially critical determinant of host-pathogen interaction. Clemens DL, Lee BY, Horwitz MA. (J Bacteriol. 1995;177(19):5644-52)
- Solution structure of Mycobacterium tuberculosis NmtR in the apo-state: insights into Ni(II)-mediated allostery. Lee CW, et al. (Biochemistry. 2012)
- Pathogenicity and virulence of Mycobacterium tuberculosis. Rahlwes KC, et al. (Virulence. 2023)
- Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis. Nemeth E, Ganz T. (Int J Mol Sci. 2021)
- Lactoferrin corrects iron-overload susceptibility to tuberculosis. Schaible UE, et al. (J Exp Med. 2002)
- Sputum microbiota in tuberculosis as revealed by 16S rRNA pyrosequencing. Cheung MK, et al. (PLoS One. 2013)
- Airway microbiome signature discriminates M. tuberculosis infection status. Kayongo A, et al. (iScience. 2024)
- Enrichment of the lung microbiome with oral taxa drives a Th17 inflammatory phenotype. Segal LN, et al. (Nat Microbiol. 2016)
- Diabetes, short-chain fatty acids and increased tuberculosis susceptibility. Lachmandas E, et al. (J Diabetes Res. 2016)
- The microbiome and the gut-lung axis in tuberculosis. Alvarado-Pena N, et al. (Front Microbiol. 2023) [Review]
- N-acetylcysteine exhibits potent anti-mycobacterial activity. Amaral EP, et al. (BMC Microbiol. 2016)
- Adjunctive N-Acetylcysteine and Lung Function in Pulmonary Tuberculosis. Wallis RS, et al. (NEJM Evid. 2024)
- Vitamin D3 induces autophagy in human macrophages via cathelicidin. Yuk JM, et al. (Cell Host Microbe. 2009)
- Adjunctive vitamin D in tuberculosis treatment: meta-analysis of individual participant data. Jolliffe DA, et al. (Eur Respir J. 2019)
- Arginine as an adjuvant to chemotherapy improves clinical outcome in active tuberculosis. Schon T, et al. (Eur Respir J. 2003)
- Lactoferrin: a modulator of immunity against tuberculosis-related granulomatous pathology. Hwang SA, Actor JK. (Mediators Inflamm. 2015)
- Metformin use reverses increased mortality associated with diabetes during TB treatment. Degner NR, et al. (Clin Infect Dis. 2018)
- The impact of M. tuberculosis on the macrophage cholesterol metabolism pathway., (Front Immunol. 2024)
- Statin adjunctive therapy shortens TB treatment in mice. Dutta NK, et al. (J Antimicrob Chemother. 2016)
- The adverse effect of iron repletion on the course of certain infections. Murray MJ, et al. (Br Med J. 1978)
- Iron status and supplementation during tuberculosis. Nienaber A, et al. (Microorganisms. 2023)
Reference [1]
Reference [2]
Iron Homeostasis in Mycobacterium tuberculosis: siderophore-mediated iron uptake.
Sritharan M. J Bacteriol. 2016
View sourceReference [3]
Identification of an ABC transporter required for iron acquisition and virulence in M. tuberculosis (IrtAB).
Rodriguez GM, Smith I. J Bacteriol. 2006
View sourceReference [4]
IdeR controls iron acquisition, storage and survival in macrophages.
Gold B, Rodriguez GM, et al. Mol Microbiol. 2001
View sourceReference [5]
Siderocalin (Lcn2) binds carboxymycobactins, defending against mycobacterial infection.
Holmes MA, et al. Structure. 2005
View sourceReference [6]
Tuberculosis and iron overload in Africa: a review.
Gangaidzo IT, Gordeuk VR. Cent Afr J Med. 1995
View sourceReference [7]
Iron Status Predicts Treatment Failure and Mortality in Tuberculosis Patients.
Isanaka S, et al. PLoS One. 2012
View sourceReference [8]
The M. tuberculosis DosR regulon and recovery from nonrespiring dormancy.
Leistikow RL, et al. J Bacteriol. 2010
View sourceReference [9]
M. tuberculosis relies on trace oxygen to survive hypoxic environments (obligate aerobe).
Kalia NP, et al. Cell Rep. 2023
View sourceReference [10]
Synergistic effects of NAC and first-line antibiotics in the granulomatous response to Mtb.
Teskey G, et al. Front Immunol. 2018
View sourceReference [11]
Zinc and copper toxicity in host defense against pathogens: M. tuberculosis as a model.
Neyrolles O, Mintz E, Catty P. Front Cell Infect Microbiol. 2013
View sourceReference [12]
Copper resistance is essential for virulence of Mycobacterium tuberculosis.
Wolschendorf F, et al. PNAS. 2011
View sourceReference [13]
Mycobacterial P1-type ATPases mediate resistance to zinc poisoning in human macrophages.
Botella H, et al. Cell Host Microbe. 2011
View sourceReference [14]
Reference [15]
SLC11A1 (NRAMP1) polymorphisms and tuberculosis susceptibility: meta-analysis.
Li X, et al. PLoS One. 2011
View sourceReference [17]
Distribution of Arsenic Resistance Genes in Prokaryotes.
Ben Fekih I, et al. Front Microbiol. 2018
View sourceReference [18]
Reference [19]
Purification, characterization, and genetic analysis of Mycobacterium tuberculosis urease, a potentially critical determinant of host-pathogen interaction.
Clemens DL, Lee BY, Horwitz MA. J Bacteriol. 1995;177(19):5644-52
View sourceReference [20]
Solution structure of Mycobacterium tuberculosis NmtR in the apo-state: insights into Ni(II)-mediated allostery.
Lee CW, et al. Biochemistry. 2012
View sourceReference [21]
Pathogenicity and virulence of Mycobacterium tuberculosis.
Rahlwes KC, et al. Virulence. 2023
View sourceReference [22]
Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis.
Nemeth E, Ganz T. Int J Mol Sci. 2021
View sourceReference [23]
Lactoferrin corrects iron-overload susceptibility to tuberculosis.
Schaible UE, et al. J Exp Med. 2002
View sourceReference [24]
Sputum microbiota in tuberculosis as revealed by 16S rRNA pyrosequencing.
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