Manganese (Mn)

Overview

Manganese shapes microbial pathogenesis by acting as a high-value cofactor for antioxidant defense and central metabolism while also becoming toxic when intracellular Mn(II) is not buffered.^[1] In the host, this creates a tug-of-war where inflammation-induced sequestration lowers Mn availability to microbes, but bursts of Mn exposure or local tissue release can flip selective pressure toward organisms with strong Mn import and detox pathways. A key driver is calprotectin, which can bind Mn and suppress growth of Mn-dependent pathogens, making “Mn starvation resistance” a recurring virulence trait.^[3] Clinically relevant niches include inflamed mucosa (colon), infected skin and wound exudate, and phagocyte-rich environments where metal withholding and oxidative stress co-occur.^[4] The most actionable leverage point is to recognize when inflammation is creating Mn restriction (favoring Mn-scavenging pathogens) versus when exposure or dysregulated supplementation is raising Mn (favoring Mn-detox phenotypes), because these two states predict different “winners” in community competition.^[5]

Chemical speciation across host niches

In blood, Mn is largely present as Mn(II) distributed between low-molecular-weight ligands and protein-bound pools, with human serum albumin providing measurable binding capacity that can buffer free Mn(II) activity and therefore microbial access.^[6] Whole-blood Mn concentrations in healthy people are commonly reported in a low microgram per liter range, but the clinical interpretability varies, which matters because “normal” systemic Mn does not directly imply “normal” luminal Mn where microbes compete. In saliva, buffering systems such as bicarbonate, phosphate, proteins and organic anions shift metal complexation and lower truly free Mn(II), so availability is governed by flow-dependent dilution and ligand load more than by total Mn alone.^[7] In gastric lumen, low pH favors soluble Mn(II) and reduces carbonate and phosphate complexation, but rapid mixing with dietary ligands can re-complex Mn in chyme before it reaches the small intestine.^[8] In the colon, Mn speciation is expected to be dominated by complexation with organic acids and microbial metabolites, making Mn “bioavailable” primarily to taxa with high-affinity importers or chelator-mediated capture rather than to passive uptake.^[9] Urine is a useful exposure matrix for total Mn measurement but is chemically heterogeneous; citrate and other ligands can lower free Mn(II) and complicate direct inference about tissue Mn stress without context.

Microbial acquisition, regulation, and buffering

Pathogens acquire and buffer Mn using dedicated importers, metallophores, regulators, maturation factors, chaperones, storage, and efflux systems, and the relative emphasis differs by niche. In Gram-negative enteric pathogens, the ABC transporter SitABCD is a well-characterized Mn/Fe acquisition system that supports growth and virulence under host-imposed metal limitation.^[10] Many bacteria also deploy NRAMP-family importers such as MntH that are optimized for Mn(II) uptake in acidic or metal-poor conditions, providing a second route when ABC uptake is constrained.^[11] Because Mn can become toxic at higher intracellular levels, exporters are not optional “luxury” genes; they are often virulence-linked because the host can present both Mn starvation and Mn intoxication pressures across different microenvironments.^[12][13] Regulation frequently centers on MntR-family metalloregulators that repress import and induce detox programs, tuning intracellular Mn to match demand from Mn enzymes such as Mn-superoxide dismutase (SodA) and Mn-dependent steps in DNA precursor synthesis.^[14]

Metal toolkit

Component class	Canonical systems/examples
Importer	MntH (NRAMP-family Mn(II) importer) supports Mn acquisition in multiple bacteria, including Bacillus and enteric organisms under limitation.[15]
Importer	SitABCD (ABC transporter) in Salmonella enterica contributes to virulence during infection, consistent with Mn/Fe limitation in vivo.[16]
Importer	MntABC (ABC-type Mn transporter) in Staphylococcus aureus is linked to pathogenic fitness in host contexts where Mn is restricted.[17]
Metallophore	Staphylopine, produced by the cnt locus in S. aureus, is a broad-spectrum metallophore; literature describes transport of multiple metals, including Mn, under some conditions, implying a potential Mn capture route when free Mn is low.[18]
Regulator	MntR (DtxR-family metalloregulator) coordinates repression of Mn import and activation of detox genes to maintain Mn homeostasis.[19]
Maturation factor	SodA (Mn-superoxide dismutase) is a key Mn-dependent antioxidant enzyme whose activity links Mn availability to oxidative stress survival during infection.[20][21]
Chaperone	Dedicated Mn trafficking proteins are less universal than for Cu or Ni; many systems rely on regulated import plus buffering by abundant ligands/proteins, leaving “true” Mn chaperones as a knowledge gap in many pathogens.[22][23]
Storage	Mn can be buffered by nonspecific ligand pools (phosphate, polyphosphate, organic acids) rather than a single canonical storage protein across taxa; this changes with pH and growth state.[24]
Efflux	MntE (Mn exporter) provides Mn detoxification in S. aureus and is required for full virulence in infection models, indicating Mn intoxication can occur in vivo.[25]
Efflux	MntP (Mn efflux) in Escherichia coli protects against Mn toxicity, illustrating that enteric bacteria must actively export Mn when exposure spikes.[26]

Nutritional immunity and host sequestration

Host proteins restrict Mn to limit microbial growth and to disable Mn-dependent enzymes that support oxidative stress resistance. The most mechanistically grounded example is calprotectin (S100A8/S100A9), which binds Mn and Zn and can suppress pathogen proliferation by starving Mn-dependent systems in inflamed tissues.^[27][28] In staphylococcal infection contexts, host calprotectin imposes Mn starvation pressure, and bacterial regulatory networks that resist this pressure are directly tied to fitness, underscoring that Mn withholding is not incidental but an antimicrobial strategy.^[29][30] At the same time, systemic proteins such as serum albumin can bind Mn with measurable affinity, contributing to a circulating buffer that may reduce spikes of free Mn(II) but also complicate attempts to infer “microbial Mn access” from total Mn measurements alone.^[31] Clinically, this means that inflamed sites with high calprotectin can create a selective filter for organisms that either import Mn at very low free concentrations, switch to alternative metal-independent enzymes, or upregulate detox and repair pathways that reduce the Mn requirement under oxidative stress.^[32]

Host sequestration map

Host factor	Microbial consequence
Calprotectin (S100A8/S100A9)	Sequesters Mn and Zn in inflamed sites, reducing Mn availability for Mn enzymes such as SodA and constraining growth of Mn-dependent pathogens.[33]
Neutrophil-rich exudate milieu	Co-localizes oxidative stress with metal withholding, increasing the fitness value of Mn-dependent antioxidant systems and high-affinity Mn acquisition.[34]
Serum albumin	Provides Mn-binding sites (reported KD on the order of micromolar), buffering free Mn(II) and potentially lowering microbial access in blood-like fluids.[35]
Histidine and amino acid pools	Compete for Mn(II) binding and reduce free Mn(II), shifting advantage toward transporters with high affinity or ligand-specific capture strategies.[36]
Citrate pool	Chelates divalent metals and can lower free Mn(II) activity in urine and intestinal fluids, altering the effective dose seen by microbes.[37]

Metallophores and community competition

Secreted chelators shift competition by lowering free Mn(II) and redistributing Mn toward organisms that can capture metal-ligand complexes. In S. aureus, the cnt locus supports production and uptake of the metallophore staphylopine, and mechanistic literature describes it as a promiscuous metal carrier whose transported metal can vary with conditions, creating a flexible response when host sequestration changes the “available” metal landscape.^[38] Even when a metallophore is better known for Zn or Ni acquisition, its ecological role can still influence Mn competition indirectly by allowing a pathogen to meet other metal needs, preserving intracellular reductant and transporter capacity for Mn acquisition during inflammation.^[39][40] Community-level effects follow from this: metallophore producers can privatize metal access, while non-producers may exploit if they carry compatible uptake components, altering which taxa dominate under metal restriction.^[41] Inflammatory cues that increase calprotectin and related nutritional immunity signals tend to upregulate bacterial metal acquisition programs, including metallophore pathways in organisms that encode them, tightening competition precisely when pathogens need Mn for oxidative stress defense.^[42][43]

Metallophores and capture

Metallophore or ligand complex	Capture system and ecological effect
Staphylopine–metal complexes	Imported via Cnt-associated systems in S. aureus; broad metal scope enables competitive advantage in chelating host environments and may include Mn under some conditions.[44][45]
Diet-derived organic acid–Mn(II) complexes	Favor microbes with transporters that tolerate ligand-bound Mn or that acidify microenvironments to increase free Mn(II) locally.[46][47]
Phosphate/polyphosphate–Mn buffering	Can reduce free Mn(II) and blunt toxicity peaks, benefiting taxa with efficient Mn exporters by preventing intracellular overload when uptake continues.[48]
Mucosal chelation milieu during inflammation	Strengthens selection for high-affinity Mn importers (MntH, ABC systems) and for regulatory programs that resist calprotectin-induced Mn starvation.[49][50]

Mismetallation and cross-metal crosstalk

When Mn rises relative to competing metals such as Fe and Zn, enzymes with permissive metal-binding sites can mis-bind, producing loss of function or altered reactivity; when Mn falls, Mn-dependent enzymes become apo or are forced onto suboptimal metals, also reducing function.^[51] A clinically relevant crosstalk pattern is that Zn stress can perturb Mn handling: in some streptococcal systems, Zn intoxication and Mn restriction interact through shared transport and regulatory circuitry, creating mixed-metal phenotypes that matter during inflammation where multiple metals shift simultaneously.^[52][53] On the other side, Mn detox genes are not only “anti-toxicity” but also “anti-mismetallation,” because exporting excess Mn prevents inappropriate occupancy of sites that should bind other metals, especially under high-exposure scenarios.^[54][55] This informs combination strategies: interventions that add Zn or alter Fe availability can unintentionally raise Mn demand or increase the fitness advantage of Mn scavengers, so a metal-aware design should anticipate whether the intervention shifts the ratio of Mn to other transition metals rather than changing Mn alone.^[56]

Mismetallation map

At-risk enzyme class	Likely wrong-metal outcome
Metalloregulators (DtxR/MntR family)	Mis-sensing can occur if non-cognate metals occupy regulatory sites, leading to inappropriate repression of import or failure to induce detox.[57]
Oxidative stress enzymes (SOD family)	Low Mn can reduce MnSOD activity, increasing oxidative damage in inflamed niches; excess Mn can drive compensatory export programs that alter fitness.[58]
Broad-specificity ABC solute-binding proteins	Competition among divalent cations can shift which metal is transported, altering intracellular metal ratios and downstream enzyme metalation.[59]
Metal-dependent transcriptional networks	Mixed-metal inflammation can create co-regulation states where Zn, Fe, and Mn programs are all induced, complicating interpretation of single-metal supplementation.[60]

Virulence pathway mapping

In S. aureus, Mn homeostasis is tied to virulence through a dual pressure model: the pathogen must import Mn under calprotectin-driven starvation yet export Mn when intracellular Mn becomes toxic, and disruption of the exporter gene mntE reduces virulence in infection models.^[61] Mn also supports antioxidant defense via Mn-dependent superoxide dismutase activity, helping pathogens survive the oxidative burst that co-occurs with nutritional immunity.^[62][63] In enteric infection, Salmonella enterica uses SitABCD to acquire Mn and Fe in the host, consistent with the need to maintain metal-dependent metabolism and stress resistance during colonization and systemic spread.^[64] A practical clinical leverage point is that Mn pressure can be inferred indirectly: environments rich in neutrophils and calprotectin suggest Mn restriction, predicting selection for Mn-scavenging and Mn-starvation-resistance programs; conversely, exposure contexts (contaminated water, dysregulated supplementation, parenteral nutrition) can raise Mn and favor Mn-export and detox phenotypes.^[65]

Virulence targets to MBTIs

Targetable node	MBTI concept with predicted effect on pathogenesis
Mn importers (MntH, SitABCD, MntABC)	Reduce Mn acquisition under host restriction to blunt MnSOD-supported oxidative stress survival; risk is collateral selection for alternative importers.[66][67]
Mn exporter MntE and its regulation	Inhibit detox only when Mn intoxication is the dominant pressure (high-exposure niches), potentially sensitizing pathogens to Mn-driven stress.[68]
Calprotectin resistance programs (regulatory adaptation)	Target bacterial regulators that specifically increase Mn-starvation resistance, shifting competition back toward commensals during inflammation.[69][70]
Metallophore capture (cnt locus)	Block staphylopine production or uptake to reduce metal capture in chelating host environments; predicted strongest effect when metal withholding is high.[71]

Exposure to microbiome outcomes

At high experimental exposures, Mn can perturb gut community structure and metabolites in animal models, with reported sex-specific shifts in microbiome composition and metabolome signatures in mice exposed to Mn(II).^[72] In a separate rodent exposure paradigm using MnCl₂ in drinking water at 200 mg/L for several weeks, microbiome remodeling was implicated in downstream neuroinflammatory or neurotoxicity phenotypes, and fecal microbiome transplantation was reported to attenuate Mn-associated outcomes, supporting a mechanistic gut-mediated component.^[73][74] In humans, quantitative metal profiling studies in early life indicate that manganese is part of milk or blood metal mixtures associated with infant gut microbiota patterns, highlighting a plausible route by which modest variations in Mn exposure during development may bias colonization dynamics.^[75] In pregnancy-associated human data, placental manganese levels have been analyzed alongside maternal gut microbiota and clinical outcomes (preeclampsia context), providing another quantitative human anchor for Mn–microbiome associations, though the directionality and causality remain uncertain.^[76]

Exposure thresholds to selection signals

Exposure or concentration range	Observed/predicted microbiome selection signal
Drinking water Mn around 0.16 to 0.61 mg/L in child exposure contexts (estimated intake differences reported)	Predicted shift toward Mn-tolerant taxa and altered metal competition signals, especially where dietary ligands are low; human microbiome outcomes are still under-characterized at these levels.[77]
Rodent drinking water MnCl₂ 200 mg/L for ~5 weeks	Dysbiosis with functional and inflammatory signatures; transplantation experiments suggest the microbiome can modulate downstream toxicity phenotypes.[78][79]
Early-life metal exposures measured by ICP-MS in milk or infant serum	Correlations between metal profiles (including Mn) and infant gut taxa abundance patterns, consistent with metal availability shaping early colonization.[80]

Antimicrobial resistance co-selection

Chronic metal exposures can co-select antibiotic resistance through co-resistance (genes linked on mobile elements), cross-resistance (shared efflux or stress pathways), and co-regulation (metal and antibiotic responses controlled together), and modern syntheses treat metals as credible long-term selection pressures in environmental reservoirs.^[81] Mn-specific evidence is less standardized than for Cu or Zn, but Mn mining and Mn-impacted environments have been associated with enrichment and transmission of antibiotic resistance genes across ecological chains, consistent with a “metal-stressed reservoir” that can seed resistomes.^[82] Importantly, not all Mn-linked signals imply increased AMR risk; engineered or natural Mn(II) bio-oxidation processes in water treatment contexts have been reported to reduce antibiotic contamination and mitigate some resistance-associated signals, highlighting that Mn chemistry can either amplify or dampen resistome pressure depending on form and context.^[83] Clinically, the most defensible stance is to treat sustained Mn hotspots (mining, contaminated well water, industrial settings) as potential co-stressors that stabilize stress-tolerant, mobile-element-rich communities, while recognizing that direct causal links to specific antibiotic resistance phenotypes in the human gut remain a priority measurement gap.^[84][85]

AMR co-selection signals

Metal exposure context	Co-selected resistance phenotype/regulon
Manganese mine or Mn-impacted agricultural soil chains	Enrichment and dissemination of ARGs along exposure chains, consistent with metal-driven stress selection in the environment.[86]
Mixed metal and antibiotic contamination in water infrastructure	Metal-associated stress responses and mobile element dynamics can support ARG persistence; Mn chemistry can interact with treatment to reduce or redistribute risk.[87]
High Mn selection pressure in bacterial culture	Selection for enhanced metal efflux and oxidative stress programs that may indirectly cross-protect against some antibiotics via generalized stress tolerance.[88]
Declining exposure after chronic contamination	Persistence of co-selected elements is expected because mobile elements and stabilized community structures can outlast the original metal driver.[89]

Assays and decision use

Measure Mn in whole blood, plasma, or urine using validated elemental analysis platforms (ICP-MS is common; atomic absorption methods remain usable), but interpretation should account for matrix effects and the limited specificity of single time-point values for microbial Mn availability.^[90] Whole-blood reference ranges are often cited and can be used to flag potential deficiency or excess, yet authoritative clinical summaries emphasize variability and pre-analytical pitfalls, so Mn results are most useful when paired with exposure history and a clinical syndrome consistent with Mn imbalance.^[91] In exposure studies or trials aiming to link Mn to microbiome outcomes, stool metal measurement by ICP-MS provides a more direct luminal signal than blood, but it still conflates unabsorbed dietary Mn, secreted Mn, and ligand-bound Mn that may not be equally bioavailable to microbes.^[92][93] Decision use in microbiome-facing contexts therefore centers on distinguishing “restriction states” (high calprotectin inflammation, likely low free Mn) from “exposure states” (high intake or accumulation, likely higher Mn load), then choosing sampling matrices that match the niche of interest (stool for colon, wound fluid for skin lesions, blood for systemic accumulation risk).^[94]

Assays to decision use

Assay and specimen	Decision use
ICP-MS, whole blood	Screen for systemic Mn excess or deficiency using reference ranges, but interpret with exposure context and high variability in mind.[95]
Electrothermal AAS, urine or whole blood	Practical alternative for Mn quantification; useful for exposure tracking when ICP-MS is unavailable, with attention to modifiers and matrix effects.[96]
ICP-MS, stool	Closest proxy for colon luminal Mn load; interpret alongside diet and inflammation markers because ligand-bound Mn may not be bioavailable.[97][98]
Calprotectin (fecal), paired with stool metals	Operationally classifies Mn restriction pressure (inflammation high) versus exposure pressure (metals high), improving prediction of which microbial toolkit will be selected.[99][100]

Body-site biogeography

At saliva, Mn availability is shaped by flow-dependent dilution and ligand buffering, so short-term changes (hydration, stimulation) may matter more than total Mn, and oral community effects are expected to favor taxa with robust Mn uptake under fluctuating pH and phosphate conditions.^[101] In the gastric lumen, low pH favors soluble Mn(II), making this a transient “high-availability” compartment that can seed downstream Mn exposure to small intestine microbes depending on diet and chelators.^[102] In the small intestine and colon, competition is dominated by transport kinetics and chelation: inflammation-driven calprotectin can impose Mn restriction, selecting for Mn-scavenging virulence programs, while dietary or water Mn can increase luminal Mn and select for exporters and detox phenotypes.^[103][104] In the blood, Mn is buffered by proteins such as albumin, and systemic accumulation risk is most clinically relevant in specialized settings (for example, long-term parenteral nutrition) rather than a routine diet.^[105] In urine, Mn provides an exposure readout but is not a direct indicator of gut Mn ecology without concurrent stool and inflammation data.^[106] At wound exudate, neutrophils and calprotectin create simultaneous Mn restriction and oxidative stress, favoring pathogens that couple Mn import, Mn-dependent antioxidant enzymes, and tightly regulated detox systems.^[107][108]

Site to interaction of interest

Body site	Interaction
Saliva	Ligand-buffered Mn with flow dependence; monitor for conditions that alter salivary composition and pH when interpreting oral microbiome shifts.[109]
Gastric lumen	Low pH increases soluble Mn(II) transiently; cue is dietary chelator load that may re-complex Mn before small intestine transit.[110]
Small intestine	Absorption and ligand exchange create dynamic Mn gradients.[111]
Colon	Inflammation can impose Mn restriction via calprotectin while exposure can raise Mn load.[112][113]
Blood	Protein buffering (albumin) and systemic monitoring are relevant for accumulation risk contexts.[114]
Urine	Exposure biomarker with matrix complexity.[115]

MBTIs and clinical strategies

Use microbiome-targeted strategies to alter Mn access and to pair with cross-metal strategies when the dominant pressure is known. In Mn restriction states (high calprotectin inflammation), the priority is to avoid inadvertently strengthening pathogen Mn acquisition, for example by adding chelators that primarily bind other metals and shift competition toward Mn-scavenging virulence programs; instead, focus on reducing inflammation drivers that create sustained Mn starvation niches.^[116][117] In Mn exposure states (high intake, contaminated well water, accumulation risk), prioritize reducing luminal Mn load and limiting selection for Mn detox phenotypes by addressing the exposure source and considering dietary ligand modulation that lowers free Mn(II) without broadly starving beneficial taxa of other essential metals.^[118] If a pathogen relies on specific Mn import or detox nodes (for example S. aureus Mn homeostasis involving MntABC and MntE), targeted inhibition of these systems is conceptually attractive, but combination design must anticipate redundancy (multiple importers) and crosstalk with Zn and Fe programs.^[119][120] Where early-life exposures are relevant, milk or infant serum metallomics paired with microbiome profiling can identify whether Mn is a meaningful covariate within a metal mixture, guiding safer supplementation strategies rather than pursuing Mn changes in isolation.^[121][122]

Intervention to expected microbial effect

Intervention	Expected microbial or host-niche effect
Source control for Mn in drinking water (filtration, alternative supply)	Lowers chronic Mn exposure pressure that can drive dysbiosis in animal models; human microbiome outcomes at common exposure levels remain under-measured.[123]
Pair stool metals with fecal calprotectin in trials	Distinguishes Mn exposure versus Mn restriction states, improving prediction of which Mn toolkit traits will be selected; does not resolve Mn speciation directly.[124][125]
Dietary ligand modulation (citrate, phytate, fiber-linked organic acids)	May lower free Mn(II) activity in the colon and reduce selection for Mn detox phenotypes; risk is unintended binding or malabsorption effects for other metals.[126][127]
Targeted anti-virulence against Mn homeostasis (import or efflux inhibitors)	Predicted to weaken pathogens in niches where Mn handling is virulence-linked; redundancy across importers and mixed-metal crosstalk can reduce efficacy.[128][129]
Early-life metallomics-informed supplementation	Uses quantitative milk or serum metals to avoid unnecessary Mn elevation in sensitive windows associated with microbiome patterning; causality is still being established.[130]

Knowledge gaps and priorities

Key uncertainties include how Mn speciation, not just total Mn, differs across colon micro-niches during inflammation, which directly controls whether high-affinity importers like MntH provide a decisive advantage.^[131][132] A second gap is identifying the dominant Mn trafficking and buffering mechanisms inside host-adapted pathogens beyond known importers and exporters, because these internal handling steps likely determine both virulence and mismatch-metal risk under mixed-metal inflammation.^[133] A third gap is quantifying human dose–response relationships between realistic Mn exposures (including drinking water ranges) and gut microbiome function and resistome trajectories, since animal models show clear perturbations but human causal data remain sparse.^[134] The most informative priorities are paired measurements of stool Mn (total and ideally fractionated), fecal inflammation markers (including calprotectin), and metagenomic pathway readouts for Mn homeostasis genes (import, efflux, metallophore loci) in cohorts stratified by exposure source and inflammatory state.^[135][136]

Research Feed

Update History

References

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39. The Metallophore Staphylopine Enables Staphylococcus aureus To Compete with the Host for Zinc and Overcome Nutritional Immunity.. Grim KP, San Francisco B, Radin JN, Brazel EB, Kelliher JL, Párraga Solórzano PKKim PC, McDevitt CA, Kehl-Fie TE.2017.. (mBio8:10.1128/mbio.01281-17.)
40. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
41. A landscape of metallophore synthesis and uptake potential of the genus Staphylococcus.. Witte Paz, M., Bitzer, A., Nieselt, K., & Heilbronner, S. (2025).. (NAR Genomics and Bioinformatics, 7(4).)
42. The Two-Component System ArlRS and Alterations in Metabolism Enable Staphylococcus aureus to Resist Calprotectin-Induced Manganese Starvation.. Radin JN, Kelliher JL, Párraga Solórzano PK, Kehl-Fie TE (2016). (PLoS Pathog 12(11): e1006040.)
43. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
44. Mechanistic Insights into Staphylopine-Mediated Metal Acquisition. Song, Liqiang, Yifei Zhang, Weizhong Chen, Tongnian Gu, Shu-Yu Zhang, and Quanjiang Ji.. (Proceedings of the National Academy of Sciences of the United States of America 115, no. 15 (2018): 3942–47.)
45. The Metallophore Staphylopine Enables Staphylococcus aureus To Compete with the Host for Zinc and Overcome Nutritional Immunity.. Grim KP, San Francisco B, Radin JN, Brazel EB, Kelliher JL, Párraga Solórzano PKKim PC, McDevitt CA, Kehl-Fie TE.2017.. (mBio8:10.1128/mbio.01281-17.)
46. Speciation analysis and fractionation of manganese: A review.. Grygo-Szymanko, E., Tobiasz, A., & Walas, S. (2016).. (TrAC Trends in Analytical Chemistry, 80, 112-124.)
47. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
48. The Escherichia coli Small Protein MntS and Exporter MntP Optimize the Intracellular Concentration of Manganese.. Martin JE, Waters LS, Storz G, Imlay JA (2015). (PLoS Genet 11(3): e1004977.)
49. Nutrient Metal Sequestration by Calprotectin Inhibits Bacterial Superoxide Defense, Enhancing Neutrophil Killing of Staphylococcus aureus.. Kehl-Fie, T. E., Chitayat, S., Hood, M. I., Damo, S., Restrepo, N., Garcia, C., Munro, K. A., Chazin, W. J., & Skaar, E. P. (2011).. (Cell Host & Microbe, 10(2), 158-164.)
50. The Two-Component System ArlRS and Alterations in Metabolism Enable Staphylococcus aureus to Resist Calprotectin-Induced Manganese Starvation.. Radin JN, Kelliher JL, Párraga Solórzano PK, Kehl-Fie TE (2016). (PLoS Pathog 12(11): e1006040.)
51. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
52. Zinc sequestration by human calprotectin facilitates manganese binding to the bacterial solute-binding proteins PsaA and MntC.. Rosen, T., Hadley, R. C., Bozzi, A. T., Ocampo, D., Shearer, J., & Nolan, E. M. (2022).. (Metallomics, 14(2).)
53. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
54. The Escherichia coli Small Protein MntS and Exporter MntP Optimize the Intracellular Concentration of Manganese.. Martin JE, Waters LS, Storz G, Imlay JA (2015). (PLoS Genet 11(3): e1004977.)
55. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
56. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
57. Structural analysis of the manganese transport regulator MntR from Bacillus halodurans in apo and manganese bound forms.. Lee MY, Lee DW, Joo HK, Jeong KH, Lee JY (2019). (PLoS ONE 14(11): e0224689.)
58. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
59. Acquisition of Mn(II) in Addition to Fe(II) Is Required for Full Virulence of Salmonella enterica Serovar Typhimurium.. Boyer E, Bergevin I, Malo D, Gros P, Cellier MFM2002.. (Infect Immun70:.)
60. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
61. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
62. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
63. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
64. Acquisition of Mn(II) in Addition to Fe(II) Is Required for Full Virulence of Salmonella enterica Serovar Typhimurium.. Boyer E, Bergevin I, Malo D, Gros P, Cellier MFM2002.. (Infect Immun70:.)
65. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
66. Acquisition of Mn(II) in Addition to Fe(II) Is Required for Full Virulence of Salmonella enterica Serovar Typhimurium.. Boyer E, Bergevin I, Malo D, Gros P, Cellier MFM2002.. (Infect Immun70:.)
67. The Staphylococcus aureus ABC-Type Manganese Transporter MntABC Is Critical for Reinitiation of Bacterial Replication Following Exposure to Phagocytic Oxidative Burst.. Coady A, Xu M, Phung Q, Cheung TK, Bakalarski C, Alexander MK, et al. (2015). (PLoS ONE 10(9): e0138350.)
68. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
69. The Two-Component System ArlRS and Alterations in Metabolism Enable Staphylococcus aureus to Resist Calprotectin-Induced Manganese Starvation.. Radin JN, Kelliher JL, Párraga Solórzano PK, Kehl-Fie TE (2016). (PLoS Pathog 12(11): e1006040.)
70. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
71. The Metallophore Staphylopine Enables Staphylococcus aureus To Compete with the Host for Zinc and Overcome Nutritional Immunity.. Grim KP, San Francisco B, Radin JN, Brazel EB, Kelliher JL, Párraga Solórzano PKKim PC, McDevitt CA, Kehl-Fie TE.2017.. (mBio8:10.1128/mbio.01281-17.)
72. Manganese-induced sex-specific gut microbiome perturbations in C57BL/6 mice.. Chi, L., Gao, B., Bian, X., Tu, P., Ru, H., & Lu, K. (2017).. (Toxicology and Applied Pharmacology, 331, 142-153.)
73. Fecal microbiome transplantation attenuates manganese-induced neurotoxicity through regulation of the apelin signaling pathway by inhibition of autophagy in mouse brain.. Liu, J., Zhang, X., Ta, X., Luo, M., Chang, X., & Wang, H. (2022).. (Ecotoxicology and Environmental Safety, 242, 113925.)
74. The gut microbiota attenuate neuroinflammation in manganese exposure by inhibiting cerebral NLRP3 inflammasome.. Wang, H., Yang, F., Xin, R., Cui, D., He, J., Zhang, S., & Sun, Y. (2020).. (Biomedicine & Pharmacotherapy, 129, 110449.)
75. Association between infants’ serum levels of 26 metals and gut microbiota: A hospital-based cross-sectional study in China.. Yan, X., Qiu, J., Huang, R., Peng, X., Xiang, S. T., Zhao, K., Peng, Y., Zhuang, Y., Ma, Y., Wu, M., & Yang, F. (2025).. (Frontiers in Microbiology, 16, 1669475.)
76. Association of placental manganese levels, maternal gut microbiota, and preeclampsia: A tripartite perspective.. Ding, T., Huang, X., Ai, S., Pu, Y., Zhao, W., He, S., & Dang, Y. (2025).. (Frontiers in Microbiology, 16, 1674549.)
77. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
78. The gut microbiota attenuate neuroinflammation in manganese exposure by inhibiting cerebral NLRP3 inflammasome.. Wang, H., Yang, F., Xin, R., Cui, D., He, J., Zhang, S., & Sun, Y. (2020).. (Biomedicine & Pharmacotherapy, 129, 110449.)
79. Fecal microbiome transplantation attenuates manganese-induced neurotoxicity through regulation of the apelin signaling pathway by inhibition of autophagy in mouse brain.. Liu, J., Zhang, X., Ta, X., Luo, M., Chang, X., & Wang, H. (2022).. (Ecotoxicology and Environmental Safety, 242, 113925.)
80. Association between infants’ serum levels of 26 metals and gut microbiota: A hospital-based cross-sectional study in China.. Yan, X., Qiu, J., Huang, R., Peng, X., Xiang, S. T., Zhao, K., Peng, Y., Zhuang, Y., Ma, Y., Wu, M., & Yang, F. (2025).. (Frontiers in Microbiology, 16, 1669475.)
81. Unravelling the mechanisms of antibiotic and heavy metal resistance co-selection in environmental bacteria.. Gillieatt, B. F., & Coleman, N. V. (2024).. (FEMS Microbiology Reviews, 48(4).)
82. Diffusion and enrichment of high-risk antibiotic resistance genes (ARGs) via the transmission chain (mulberry leave, guts and feces of silkworm, and soil) in an ecological restoration area of manganese mining, China: Role of heavy metals.. Yan, K., Wei, M., Li, F., Wu, C., Yi, S., Tian, J., Liu, Y., & Lu, H. (2023).. (Environmental Research, 225, 115616.)
83. Simultaneous antibiotic removal and mitigation of resistance induction by manganese bio-oxidation process.. Ren, C., Xu, Q., Alvarez, P. J., Zhu, L., & Zhao, H. (2023).. (Water Research, 244, 120442.)
84. Unravelling the mechanisms of antibiotic and heavy metal resistance co-selection in environmental bacteria.. Gillieatt, B. F., & Coleman, N. V. (2024).. (FEMS Microbiology Reviews, 48(4).)
85. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
86. Diffusion and enrichment of high-risk antibiotic resistance genes (ARGs) via the transmission chain (mulberry leave, guts and feces of silkworm, and soil) in an ecological restoration area of manganese mining, China: Role of heavy metals.. Yan, K., Wei, M., Li, F., Wu, C., Yi, S., Tian, J., Liu, Y., & Lu, H. (2023).. (Environmental Research, 225, 115616.)
87. Simultaneous antibiotic removal and mitigation of resistance induction by manganese bio-oxidation process.. Ren, C., Xu, Q., Alvarez, P. J., Zhu, L., & Zhao, H. (2023).. (Water Research, 244, 120442.)
88. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
89. Unravelling the mechanisms of antibiotic and heavy metal resistance co-selection in environmental bacteria.. Gillieatt, B. F., & Coleman, N. V. (2024).. (FEMS Microbiology Reviews, 48(4).)
90. Determination of Manganese in Urine and Whole Blood Samples by Electrothermal Atomic Absorption Spectrometry: Comparison ofChemical Modifiers. Frederico Garcia PINTO, Ulisses Villela REY, Eduardo Freitas FERNANDES, Josianne Nicácio SILVEIRA, Leiliane AMORIM, and José Bento Borba da SILVA. (ANALYTICAL SCIENCES DECEMBER 2006, VOL. 22)
91. Investigative algorithms for disorders affecting plasma manganese concentration: a narrative review.. Breen J, Shipman AR.. (J Lab Precis Med 2025;10:24.)
92. Association between infants’ serum levels of 26 metals and gut microbiota: A hospital-based cross-sectional study in China.. Yan, X., Qiu, J., Huang, R., Peng, X., Xiang, S. T., Zhao, K., Peng, Y., Zhuang, Y., Ma, Y., Wu, M., & Yang, F. (2025).. (Frontiers in Microbiology, 16, 1669475.)
93. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
94. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
95. Investigative algorithms for disorders affecting plasma manganese concentration: a narrative review.. Breen J, Shipman AR.. (J Lab Precis Med 2025;10:24.)
96. Determination of Manganese in Urine and Whole Blood Samples by Electrothermal Atomic Absorption Spectrometry: Comparison ofChemical Modifiers. Frederico Garcia PINTO, Ulisses Villela REY, Eduardo Freitas FERNANDES, Josianne Nicácio SILVEIRA, Leiliane AMORIM, and José Bento Borba da SILVA. (ANALYTICAL SCIENCES DECEMBER 2006, VOL. 22)
97. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
98. Association between infants’ serum levels of 26 metals and gut microbiota: A hospital-based cross-sectional study in China.. Yan, X., Qiu, J., Huang, R., Peng, X., Xiang, S. T., Zhao, K., Peng, Y., Zhuang, Y., Ma, Y., Wu, M., & Yang, F. (2025).. (Frontiers in Microbiology, 16, 1669475.)
99. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
100. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
101. The buffer capacity and buffer systems of human whole saliva measured without loss of CO2.. Bardow, A., Moe, D., Nyvad, B., & Nauntofte, B. (2000).. (Archives of Oral Biology, 45(1), 1-12.)
102. Speciation analysis and fractionation of manganese: A review.. Grygo-Szymanko, E., Tobiasz, A., & Walas, S. (2016).. (TrAC Trends in Analytical Chemistry, 80, 112-124.)
103. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
104. Manganese-induced sex-specific gut microbiome perturbations in C57BL/6 mice.. Chi, L., Gao, B., Bian, X., Tu, P., Ru, H., & Lu, K. (2017).. (Toxicology and Applied Pharmacology, 331, 142-153.)
105. Studies on manganese complexes of human serum albumin.. Chapman, B., MacDermott, T., & O'Sullivan, W. (1973).. (Bioinorganic Chemistry, 3(1), 27-38.)
106. Determination of Manganese in Urine and Whole Blood Samples by Electrothermal Atomic Absorption Spectrometry: Comparison ofChemical Modifiers. Frederico Garcia PINTO, Ulisses Villela REY, Eduardo Freitas FERNANDES, Josianne Nicácio SILVEIRA, Leiliane AMORIM, and José Bento Borba da SILVA. (ANALYTICAL SCIENCES DECEMBER 2006, VOL. 22)
107. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
108. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
109. The buffer capacity and buffer systems of human whole saliva measured without loss of CO2.. Bardow, A., Moe, D., Nyvad, B., & Nauntofte, B. (2000).. (Archives of Oral Biology, 45(1), 1-12.)
110. Speciation analysis and fractionation of manganese: A review.. Grygo-Szymanko, E., Tobiasz, A., & Walas, S. (2016).. (TrAC Trends in Analytical Chemistry, 80, 112-124.)
111. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
112. Nutrient Metal Sequestration by Calprotectin Inhibits Bacterial Superoxide Defense, Enhancing Neutrophil Killing of Staphylococcus aureus.. Kehl-Fie, T. E., Chitayat, S., Hood, M. I., Damo, S., Restrepo, N., Garcia, C., Munro, K. A., Chazin, W. J., & Skaar, E. P. (2011).. (Cell Host & Microbe, 10(2), 158-164.)
113. Manganese-induced sex-specific gut microbiome perturbations in C57BL/6 mice.. Chi, L., Gao, B., Bian, X., Tu, P., Ru, H., & Lu, K. (2017).. (Toxicology and Applied Pharmacology, 331, 142-153.)
114. Studies on manganese complexes of human serum albumin.. Chapman, B., MacDermott, T., & O'Sullivan, W. (1973).. (Bioinorganic Chemistry, 3(1), 27-38.)
115. Determination of Manganese in Urine and Whole Blood Samples by Electrothermal Atomic Absorption Spectrometry: Comparison ofChemical Modifiers. Frederico Garcia PINTO, Ulisses Villela REY, Eduardo Freitas FERNANDES, Josianne Nicácio SILVEIRA, Leiliane AMORIM, and José Bento Borba da SILVA. (ANALYTICAL SCIENCES DECEMBER 2006, VOL. 22)
116. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
117. The Two-Component System ArlRS and Alterations in Metabolism Enable Staphylococcus aureus to Resist Calprotectin-Induced Manganese Starvation.. Radin JN, Kelliher JL, Párraga Solórzano PK, Kehl-Fie TE (2016). (PLoS Pathog 12(11): e1006040.)
118. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
119. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
120. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
121. Human milk metals and metalloids shape infant microbiota. Eduard Flores Ventura, Manuel Bernabeu, Belén Callejón-Leblic, Raúl Cabrera-Rubio, Laxmi Yeruva, Javier Estañ-Capell, Cecilia Martínez-Costa, Tamara García-Barrera and María Carmen Collado. (Food Funct., 2024, 15, 12134-12145)
122. Association between infants’ serum levels of 26 metals and gut microbiota: A hospital-based cross-sectional study in China.. Yan, X., Qiu, J., Huang, R., Peng, X., Xiang, S. T., Zhao, K., Peng, Y., Zhuang, Y., Ma, Y., Wu, M., & Yang, F. (2025).. (Frontiers in Microbiology, 16, 1669475.)
123. Manganese-induced sex-specific gut microbiome perturbations in C57BL/6 mice.. Chi, L., Gao, B., Bian, X., Tu, P., Ru, H., & Lu, K. (2017).. (Toxicology and Applied Pharmacology, 331, 142-153.)
124. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
125. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
126. Speciation analysis and fractionation of manganese: A review.. Grygo-Szymanko, E., Tobiasz, A., & Walas, S. (2016).. (TrAC Trends in Analytical Chemistry, 80, 112-124.)
127. Regulatory effects of transition metals supplementation/deficiency on the gut microbiota.. Li, CY., Li, XY., Shen, L. et al.. (Appl Microbiol Biotechnol 105, 1007–1015 (2021).)
128. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
129. Acquisition of Mn(II) in Addition to Fe(II) Is Required for Full Virulence of Salmonella enterica Serovar Typhimurium.. Boyer E, Bergevin I, Malo D, Gros P, Cellier MFM2002.. (Infect Immun70:.)
130. Human milk metals and metalloids shape infant microbiota. Eduard Flores Ventura, Manuel Bernabeu, Belén Callejón-Leblic, Raúl Cabrera-Rubio, Laxmi Yeruva, Javier Estañ-Capell, Cecilia Martínez-Costa, Tamara García-Barrera and María Carmen Collado. (Food Funct., 2024, 15, 12134-12145)
131. Speciation analysis and fractionation of manganese: A review.. Grygo-Szymanko, E., Tobiasz, A., & Walas, S. (2016).. (TrAC Trends in Analytical Chemistry, 80, 112-124.)
132. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)
133. Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus.. Grunenwald CMChoby JEJuttukonda LJBeavers WNWeiss ATorres VJ, Skaar EP2019.. (mBio10:10.1128/mbio.02915-18.)
134. Manganese-induced sex-specific gut microbiome perturbations in C57BL/6 mice.. Chi, L., Gao, B., Bian, X., Tu, P., Ru, H., & Lu, K. (2017).. (Toxicology and Applied Pharmacology, 331, 142-153.)
135. Molecular basis for manganese sequestration by calprotectin and roles in the innate immune response to invading bacterial pathogens.. Damo SM, Kehl-Fie TE, Sugitan N, et al.. (Proc Natl Acad Sci U S A. 2013)
136. Bacterial manganese sensing and homeostasis.. Waters, L. S. (2020).. (Current Opinion in Chemical Biology, 55, 96-102.)