Nickel
Bacteria regulate transition metal levels through complex mechanisms to ensure survival and adaptability, influencing both their physiology and the development of antimicrobial strategies.
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Karen Pendergrass
Overview 
Research Feed 
References Overview
Nickel (Ni) is a ubiquitous trace metal present in soil, water, foods, and many consumer products.[1] In humans, nickel has been commonly associated with hypersensitivity reactions, particularly nickel-induced contact dermatitis. Recent studies have suggested that nickel hypersensitivity might be linked to conditions such as endometriosis and irritable bowel syndrome (IBS). While Nickel has no known essential biochemical role in humans, it is required by numerous microorganisms for key enzymes that influence metabolism and virulence.[2] Understanding these mechanisms opens pathways for potential therapeutic interventions, such as targeting nickel acquisition or the activity of these enzymes to limit pathogen survival and virulence, and improve host health.
Nickel in Microbial Metabolism and Virulence
Many pathogenic microbes rely on Ni as a cofactor for enzymes that enhance their survival and virulence. In fact, at least 39 major bacterial and 9 eukaryotic pathogens are known to require Ni for various enzymes – including urease, [NiFe] hydrogenase, Ni-dependent glyoxalase I (Ni-GloI), acireductone dioxygenase (Ni-ARD), and Ni-superoxide dismutase (Ni-SOD) – whereas human hosts do not require Ni for any enzyme.[4] This host-pathogen disparity presents a therapeutic opportunity: selective nickel sequestration—by targeting the pathogen’s unique reliance on Ni-dependent enzymes—disrupts microbial virulence while sparing host physiology, exemplifying a precise and effective form of metallomic targeting.[5] Key Ni-dependent microbial pathways include:
| Ni-dependent microbial pathways | Function |
|---|---|
| Urease | Urease is a Ni-dependent enzyme essential for acid neutralization in H. pylori, Proteus, and Klebsiella, enabling colonization of the stomach or urinary tract. In H. pylori, urease (and Ni–Fe hydrogenase) is so critical that standard therapy may fail if nickel is abundant. A pilot trial found that adding a Ni-free diet to triple therapy increased eradication rates from 46% to 85% (22/26 vs. 12/26, p<0.01). The mechanism is Ni restriction suppressing urease, lowering pH resistance and boosting antibiotic efficacy.[6] |
| [NiFe] Hydrogenase | [NiFe] hydrogenase is a Ni-dependent enzyme that enables H. pylori and Salmonella to use H₂ as an energy source and is a documented virulence factor.[7] In H. pylori, this enzyme promotes gastric colonization and growth, while ∆hyd mutants show reduced colonization (24% vs. 100%) and fail to translocate the CagA oncoprotein or induce cancer in models.[8] A low-nickel diet suppresses this pathway by depriving hydrogenase of Ni, forcing H. pylori to triage Ni between hydrogenase and urease, potentially attenuating H. pylori’s acid resistance and virulence, simultaneously.[9] |
| Acireductone Dioxygenase (ARD) | Acireductone dioxygenase (ARD) is a methionine salvage enzyme that uses either Fe²⁺ or Ni²⁺, generating different products: Ni-ARD produces toxic CO and methylthiopropionate, while Fe-ARD yields formate and a methionine precursor. Pathogenic Enterobacteriaceae and other γ-proteobacteria, including Klebsiella, Pseudomonas, and Acinetobacter, predominantly encode Ni-ARD, which is absent in eukaryotes. LNiD may shift ARD activity toward the less virulent Fe-bound form or impair ARD entirely, disrupting methionine salvage and bacterial signaling.[10] |
| Ni-Glyoxalase I (Ni-GloI) | Ni-Glyoxalase I (Ni-GloI) detoxifies methylglyoxal, a toxic byproduct, and is used by many pathogens including E. coli, Pseudomonas, Neisseria, Yersinia, and Clostridium. Unlike the Zn²⁺-dependent form found in humans, these microbes rely on Ni-GloI for survival under stress. Disrupting Ni-GloI impairs detoxification and viability, as shown in Leishmania. LNiD may reduce microbial stress tolerance by limiting Ni and re-sensitizing pathogens to their own metabolic toxins.[11] |
| Ni-Superoxide Dismutase (Ni-SOD) | Ni-Superoxide Dismutase (Ni-SOD) is a rare SOD variant found in some bacteria, such as Streptomyces spp., but not in mammals. It enables pathogens to resist oxidative bursts from immune cells. While most pathogens use Mn- or Fe-SOD, some, like Streptomyces scabies, rely specifically on Ni-SOD . LNiD may impair these pathogens’ antioxidant defenses by limiting Ni availability, reducing their resistance to host immunity. [12] |
| Biofilm Formation and Antimicrobial Resistance | Chronic nickel exposure promotes bacterial adaptation via increased adhesion, biofilm formation, and antibiotic resistance, as shown in E. coli and others. Nickel acts as a stress signal that upregulates biofilm-related genes, enhancing microbial protection. Conversely, a low-nickel diet may reduce biofilm formation by lowering Ni availability, shifting the gut microbiota away from Ni-tolerant, drug-resistant opportunists and favoring benign commensals. [13] |
| Methanogenic Archaea | Methanogenic archaea such as Methanobrevibacter smithii, linked to constipation-predominant irritable bowel syndrome IBS, require Ni-containing enzymes like methyl-coenzyme M reductase with the F430 cofactor for methanogenesis. Ni is essential for their growth, and excess Ni may drive methane production, slowing gut transit and causing bloating. A low-nickel diet suppresses these archaea and reduce methane-associated GI symptoms, though clinical evidence is still emerging. [14] |
________
Here we present a compilation of both eukaryotic and prokaryotic microorganisms featuring nickel-dependent enzymes, accompanied by their potential or established functions in various metabolic and pathogenic processes:
| Pathogen | Ni-enzyme | Role in Pathogenesis |
| EUKARYOTES | ||
| Human fungi | ||
| Cryptococcus neoformans | Ure | Acts as a critical determinant in the development of cryptococcosis, facilitates sequestration within the brain’s microvasculature, regulates the pH within phagolysosomes affecting brain infection outcomes, and is disseminated through extracellular vesicles. |
| Cryptococcus gattii | Ure | Functions as a key virulence determinant in murine models. |
| Coccidioides posadasii | Ure | Linked to the development of coccidioidomycosis in murine studies. |
| Histoplasma capsulatum | Distribution is facilitated by extracellular vesicles, a method that may impact its pathogenicity. | |
| Paracoccidioides brasiliensis | Ure | Gene expression is notably increased during infection in murine models, suggesting a role in its pathogenesis. |
| Oomycetes | ||
| Pythium insidiosum | Ure | Proposed to be a contributing factor to the pathogenicity of pythiosis. |
| Protists | ||
| Leishmania maior | Glo-l | Performs a vital function in the parasite’s metabolic process by neutralizing toxic methylglyoxal. |
| Leishmania donovani | Glo-l | Crucial for the proliferation of the parasite and posited as a potential pharmacological target, it plays a significant role in the detoxification process critical for parasite metabolism. |
| Trypanosoma cruzi | Ard Glo-l | Key for the methionine recycling process, aiding in the parasite’s metabolic functions, and detoxifies methylglyoxal, contributing to parasite maintenance. |
| PROKARYOTES | ||
| Actinobacteria | ||
| Actinomyces naeslundii | Ure | Key for adaptations to acidic conditions and is implicated in the formation of plaques. |
| Corynebacterium urealyticum | Ure | Contributes significantly to the pathology of urinary tract infections. |
| Mycobacterium tuberculosis | Hyc Ure | Integral for optimal growth and is more prominently expressed during the infection of human macrophages and in both resting and activated states of murine bone marrow macrophages, essential for survival in nitrogen-depleted conditions. |
| Streptomyces scabies | Sod | Protects against oxidative damage that occurs when encountering the host, typically a plant host. |
| Firmicutes | ||
| Clostridia | Glo-l | Its metabolic importance lies in the detoxification of methylglyoxal, aiding in maintaining the microbe’s metabolic functions. |
| Staphylococcus aureus | Ure | Shows an increase in structural and accessory gene expression in biofilm states, is necessary for the acid response and sustained infection within the murine kidney, and exhibits decreased activity in mixed-species biofilms with S. epidermidis. |
| Staphvlococcus epidermidis | Ure | Demonstrates reduced activity when present in biofilms with S. aureus, indicating a complex interplay in mixed bacterial communities. |
| Staphylococcus saprophyticus | Ure | Plays a role in the infection of the urinary bladder and the formation of bladder stones in rodent models. |
| Streptococcus salivarius | Ure | Serves as a nitrogen source and helps the bacterium withstand acidic stress. |
| Mollicutes | ||
| Ureaplasma urealyticum | Ure | Associated with infections of the human vaginal tract and participates in energy generation via proton motive force-driven ATP synthesis; also involved in the formation of struvite stones in rat models. |
| Ureaplasma parvum | Ure | Involved in human vaginal infections and used in diagnostic applications. |
| Ureaplasma diversum | Ure | Implicated in the vaginal infections of cattle and small ruminants. |
| Proteobacteria | ||
| Alphaproteobacteria | ||
| Brucella abortus | Ure | Necessary for the colonization of the intestinal tract in murine models, with urease-immunization shown to provide protective effects against Brucella infections in mice. |
| Brucella melitensis | Ure | Necessary for the colonization of the intestinal tract in murine models, with urease-immunization shown to provide protective effects against Brucella infections in mice. |
| Brucella suis | Ure | Necessary for the colonization of the intestinal tract in murine models, with urease-immunization shown to provide protective effects against Brucella infections in mice. |
| Betaproteobacteria | ||
| Neisseria meningitides | Glo-l | Hypothesized to play a role in the detoxification of methylglyoxal and the regulation of potassium efflux, potentially contributing to pathogenicity. |
| Neisseria gonorrhoeae | Glo-I | Hypothesized to play a role in the detoxification of methylglyoxal and the regulation of potassium efflux, potentially contributing to pathogenicity. |
| Gammaproteobacteria | ||
| All y-proteobacteria | Ard | Important for metabolism: methionine salvage pathway |
| All v-proteobacteria | Glo-I | Important for methylalyoxal detoxification, potassium efflux |
| Acinetobacter baumannii | Ure | Identified as a virulence factor in invertebrate hosts and essential for the survival in the gastric environment. |
| Acinetobacter Iwoffii | Ure | Identified as a virulence factor in invertebrate hosts and essential for the survival in the gastric environment. |
| Actinobacillus pleuropneumoniae | Ure Hyd-1 | Plays an essential role in respiratory infections in swine and is linked to metabolism and motility that are driven by the proton motive force. |
| Escherichia coli | Hyd-2 Hyc | Involved in metabolism and motility supported by the proton motive force and helps dissipate acidity induced by formic acid in the fermentative lactate hydrogen lyase (FHL) complex. |
| E. coli (Shiga-toxin producing) | Ure | Critical for the bacterial colonization and maintenance within the gastrointestinal tract of murine hosts. |
| Edwardsiella tarda | Hyd | The accessory protein Sip2 is critical for acid resistance and host infection. |
| Haemophilus influenzae | Ure | Its role in acid resistance is prominent during human pulmonary infections. |
| Klebsiella pneumoniae | Ure | Required for colonization in murine intestinal models. |
| Morganella morganii | Ure | Necessary for survival at low pH environments. |
| Proteus mirabilis | Hyd Ure | Facilitates swarming complex, contributes to the persistence of infection, stone formation in the urinary system, and the development of kidney infection in models; also a factor in bladder stone clusters and biofilm formation in mixed bacterial communities. |
| Providencia stuarti | Ure | Participates in the formation of crystal stones and is a component in biofilm communities involving multiple bacterial species. |
| Pseudomonas aeruginosa | Glo-I | Plays a role in methylglyoxal detoxification and is posited to be involved in potassium ion transport mechanisms, which are speculative contributions to its pathogenic profile. |
| Salmonella Typhimurium | Hyd-1 Hyd-2 Hyd-5 Hyc | Critical for surviving acidic conditions within the host and for facilitating invasion and replication within macrophages; identified as key for invasion of the gut. Active under both oxygen-rich conditions and within host immune cells; also necessary for resistance to acidic environments under anaerobic conditions. |
| Shigella flexneri | Hyd | Essential for resistance to acidic conditions, which is pivotal for its survival and virulence. |
| Vibrio parahaemolyticus | Ure | Identified as a significant mechanism contributing to its pathogenicity. |
| Yersinia enterocolitica | Ure | Necessary for survival in acidic environments. |
| Yersinia pestis | Glo-I | Plays a role in methylglyoxal detoxification and is posited to be involved in potassium ion transport mechanisms, which are speculative contributions to its pathogenic profile. |
| Deltaproteobacteria | ||
| Bilophila wadsworthia | Hyd | Utilizes hydrogen as an energy source for optimal growth, especially in environments containing hydrogen and taurine. |
| Epsilonproteobacteria | ||
| Campvlobacter jejuni | Hyd | Crucial for colonization of the chicken gastrointestinal tract; vital for chicken gut colonization in the absence of formate dehydrogenase pathways; required for interaction with human intestinal cells in vitro. |
| Campylobacter concisus | Hyd | Essential for growth in microaerobic conditions. |
| Helicobacter hepaticus | Hyd Ure | Involved in amino acid transport, which can lead to liver damage in hosts; also promotes inflammation in the liver of mice. |
| Helicobacter mustelae | Ure | Necessary for colonization of the stomach in ferrets. |
| Helicobacter pylori | Hyd Ure | Necessary for colonization of the stomach in mice; involved in the fixation of carbon monoxide; plays a role in the translocation of CagA protein into host cells, which is associated with cytotoxic effects; critical for colonization of the stomach in germ-free piglets and for inducing apoptosis in gastric cells through interaction with MHC molecules; urease by-products like CO₂ and ammonia are important for protection against host defenses and disrupting cell junction integrity; contributes to chronic infection in mice models and has roles in blood vessel formation in developmental models; implicated in inflammatory pathways in blood platelets, and also posited to have a role in oxidative stress management. |
| * Abreviations: Ard: acireductone dioxygenase; Glo-l: Glyoxalase I; Hyc: H2-evolving hydrogenase; Hyd: H2-uptake hydrogenase; Sod: superoxide dismutase; Ure: urease. Data from: Maier RJ, Benoit SL. Role of Nickel in Microbial Pathogenesis. Inorganics. 2019; 7(7):80. https://doi.org/10.3390/inorganics7070080 | ||
Host Strategies to Limit Nickel Availability
The intricacies of nickel (Ni) dynamics between pathogenic microorganisms and their hosts highlight a complex interplay of nutritional immunity, pathogen virulence mechanisms, and potential therapeutic interventions. Nickel’s essential role for specific virulence factors in pathogens, juxtaposed with its sparse availability in the host, presents both acquisition and homeostasis challenges for pathogens. This scarcity, and the host’s strategies to further limit Ni availability to pathogens, represents a critical aspect of the host-pathogen interaction and offers insights into novel antimicrobial strategies.
The host employs several strategies to restrict pathogen access to essential metals, including nickel, as a defense mechanism. The concept of nutritional immunity, where the host limits available metals to thwart pathogen growth, is well-documented for metals such as iron, zinc, and manganese. However, the mechanisms related to nickel are less understood but equally critical. Proteins like calprotectin, lactoferrin, and hepcidin play roles in sequestering metals, including nickel, thereby inhibiting the function of nickel-dependent enzymes in pathogens, such as ureases and hydrogenases. This metal sequestration limits the ability of pathogens to utilize these essential cofactors for their virulence factors, thus attenuating their infective capabilities.
—-At sites of inflammation, neutrophils deploy metal-binding proteins such as calprotectin, lipocalin, and lactoferrin to combat infection. Calprotectin, a defense protein known for its zinc-binding capability, plays a crucial role in hindering pathogen growth. Intriguingly, recent research by Nakashige et al. reveals that calprotectin exhibits a higher affinity for nickel (Ni(II)), preferring it to zinc (Zn(II)) at its hexahistidine site. This discovery underscores calprotectin’s ability to deprive pathogens, specifically S. aureus and K. pneumoniae, of nickel, impairing their urease activity in bacterial cultures and thereby inhibiting their growth.
Chelation Strategies
| Agent | Findings | Implications |
| Lactoferrin | Chelates Iron and Nickel | While the antibacterial properties of lactoferrin, a versatile globular protein, are partly due to its ability to bind iron, its histidine and tyrosine ligands also have the capacity to attach to other metals, such as nickel. Consequently, the possibility that lactoferrin can also inhibit pathogens by sequestering nickel warrants consideration. The potential nickel-sequestering effect of lactoferrin towards pathogens offers a promising avenue for antimicrobial intervention. This capability implies that lactoferrin could be used not only in the treatment of infections caused by iron-dependent pathogens but also those that rely on nickel for virulence. Further, the use of lactoferrin or its derivatives as therapeutic agents could be explored for infections where nickel-dependent enzymes play a critical role in pathogen survival and infection. |
| Dimethylglyoxime DMG | High-Affinity Nickel chelator | Preliminary Findings on dimethylglyoxime (DMG) highlight its potential as an innovative antimicrobial strategy, particularly against enteric pathogens resistant to multiple drugs. By chelating nickel, DMG effectively inhibits essential nickel-dependent enzymes like hydrogenases and ureases, impairing the growth and survival of pathogens such as multi-drug resistant strains of Salmonella Typhimurium and Klebsiella pneumoniae. The consequent decrease in pathogen virulence and colonization, as evidenced by improved survival rates in mouse and larval models, indicates DMG’s promise for therapeutic use[x]. This opens avenues for the development of nickel-chelation therapies as a novel class of antimicrobials to combat challenging bacterial infections and curb the threat posed by antibiotic resistance. |
Implications for Research and Therapeutics
Understanding the mechanisms of nickel acquisition, transport, and regulation in pathogens, alongside the characterization of nickel-dependent enzymes, offers potential avenues for developing new therapeutic strategies. Targeting nickel transport systems or the maturation and activity of nickel-dependent virulence factors could provide a novel means of combating infections, particularly for pathogens where nickel plays a crucial role in survival and pathogenicity.
The recognition that nickel-requiring enzymes are important for the virulence of a diverse array of both prokaryotic and eukaryotic pathogens emphasizes the need for further research into nickel biology in microbial pathogenesis. Investigating the potential pathogenic roles of newly identified Ni-binding components, informed by recent experimental data, can expand our understanding of microbial virulence mechanisms and reveal new targets for intervention.
The dependency of certain pathogens on nickel for vital enzymatic processes directly linked to virulence factors highlights the complex interplay between microbial metabolism and pathogenicity. The study of nickel in microbial pathogenesis not only offers insights into the basic biology of pathogens but also opens up potential therapeutic avenues aimed at disrupting metal homeostasis to combat infections.
MBTIs
Various strategies for nickel chelation may offer promise as a treatment for the aforementioned eukaryotic and prokaryotic microorganisms featuring nickel-dependent enzymes. Dimethylglyoxime has already been investigated as a potent nickel chelation therapy to combat multi-drug resistant enteric pathogens, including multi-drug resistant strains of Salmonella Typhimurium and Klebsiella pneumonia. [x]
Theoretical Foundation:
As an essential cofactor for critical enzymes such as hydrogenase and urease, Nickel has established roles in microbial pathogenic processes. However, the scope of nickel’s involvement in pathogens with other nickel-requiring enzymes warrants further exploration. Additional nickel-utilizing proteins, or those responding to nickel concentration changes, are anticipated to be identified. It is vital to address the gaps in our understanding of nickel dynamics and its regulation within pathogens that require this metal. This includes delineating the origins of dietary nickel, how host metabolism influences its availability to pathogens and the effect of host gut microbiota composition on nickel presence. Investigating these areas is crucial for advancing our knowledge.
The variability of nickel’s accessibility in the host is notable, necessitating a deeper understanding of its general availability across various organs, tissues, and cell types, such as epithelial, immune, and blood cells. One promising research direction is the unique requirement of nickel by numerous pathogens—39 prokaryotic and nine eukaryotic—unlike their mammalian hosts. This discrepancy presents the possibility of specifically targeting these pathogens through nickel sequestration strategies.
Notably, higher plants naturally employ nickel sequestration; they utilize nickel (e.g., in Ni-urease). Meanwhile, very few nickel-requiring plant pathogens exist, such as S. scabies and some Streptomyces species that possess Ni-SOD.
This interesting dichotomy—plants requiring nickel but having few nickel-dependent pathogens and mammals not requiring it yet hosting many nickel-utilizing pathogens—provides insight into the evolutionary battle for nickel between hosts and pathogens. It also suggests potential avenues for future research endeavors to inhibit or eliminate nickel-dependent pathogens in humans and other mammals through various strategies, such as employing a low-nickel diet or nickel chelation therapies.
Research Feed
Nickel chelation therapy as an approach to combat multi-drug resistant enteric pathogens
September 25, 2019
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Metals •
Metals
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This study evaluates nickel chelation therapy using DMG against multidrug-resistant Salmonella and Klebsiella. DMG impaired virulence by inhibiting Ni-dependent enzymes, reduced bacterial load in organs, and improved survival in animal models, offering a promising metallomic intervention.
What was studied?
This experimental study investigated the therapeutic potential of the nickel-specific chelator dimethylglyoxime (DMG) as an antimicrobial intervention against multidrug-resistant (MDR) enteric pathogens, specifically Salmonella enterica serovar Typhimurium and Klebsiella pneumoniae. The research assessed whether nickel chelation by DMG could inhibit the growth and virulence of these pathogens in vitro and in vivo through interference with essential Ni-dependent bacterial enzymes.
Who was studied?
The study utilized bacterial strains of MDR Klebsiella pneumoniae (ATCC BAA-2472) and MDR Salmonella Typhimurium (ATCC 700408 and ATCC 14028), in addition to two animal models: Mus musculus (mice) for assessing DMG efficacy and safety in systemic infection, and Galleria mellonella (wax moth larvae) for testing virulence attenuation in an invertebrate model.
What were the most important findings?
This study provides compelling evidence that dimethylglyoxime (DMG), a nickel-specific chelator, exerts a potent bacteriostatic effect against multidrug-resistant Salmonella Typhimurium and Klebsiella pneumoniae by inhibiting key Ni-dependent enzymes—hydrogenase and urease, respectively. At concentrations between 1 and 5 mM, DMG impaired enzyme activity without exhibiting toxicity in murine or invertebrate models. In vivo, DMG administration resulted in 50% survival among infected mice, compared to complete lethality in untreated controls, and led to a 10-fold reduction in bacterial colonization of the liver and spleen. In Galleria mellonella, pre-injection with DMG improved survival by 40–60% after challenge with lethal doses of MDR pathogens. NMR analysis confirmed DMG’s systemic absorption by detecting it in liver tissue. The absence of adverse effects in either model underscores the compound's therapeutic safety. The targeted suppression of nickel-requiring pathogens supports the utility of metallome-directed interventions in combating MDR infections, particularly for pathogens that rely on nickel-dependent enzymes for virulence.
| Finding | Details |
|---|
| Bacteriostatic Activity | DMG showed concentration-dependent inhibition (1–5 mM) of MDR S. Typhimurium and K. pneumoniae. |
| Target Enzymes | Inhibited hydrogenase activity in Salmonella and urease activity in Klebsiella, both Ni-dependent enzymes. |
| Animal Survival | 50% survival in DMG-treated mice vs. 0% in untreated controls. |
| Organ Burden Reduction | 10-fold reduction in bacterial colonization in livers and spleens of treated mice. |
| Larvae Protection | 40–60% survival in DMG-treated G. mellonella larvae following lethal bacterial challenge. |
| Systemic Bioavailability | NMR confirmed presence of DMG in liver tissue post-oral administration. |
| Safety Profile | No observed toxicity in mice or larvae at therapeutic doses. |
| Mechanistic Relevance | Aligns with a metallomic intervention strategy by targeting Ni-dependent MMAs (Salmonella, Klebsiella). |
What are the greatest implications of this study?
This study underscores the translational potential of metallome-targeted interventions, specifically through nickel chelation, as a viable therapeutic approach against MDR pathogens. By inhibiting bacterial nickel-dependent enzymatic machinery critical for virulence and survival, such as hydrogenases and ureases, DMG offers a mechanism-based strategy that bypasses conventional antibiotic resistance pathways. The fact that many high-priority MDR pathogens identified by the WHO possess Ni-dependent enzymes positions nickel chelation as a broadly applicable antimicrobial modality. Moreover, the non-toxic profile of DMG in two distinct animal models supports its development for clinical use, particularly as an adjunct or alternative to antibiotics in cases of resistant infections.
Nickel
Bacteria regulate transition metal levels through complex mechanisms to ensure survival and adaptability, influencing both their physiology and the development of antimicrobial strategies.
Endometriosis
Endometriosis involves ectopic endometrial tissue causing pain and infertility. Validated and Promising Interventions include Hyperbaric Oxygen Therapy (HBOT), Low Nickel Diet, and Metronidazole therapy.
Irritable Bowel Syndrome (IBS)
Irritable Bowel Syndrome (IBS) is a common gastrointestinal disorder characterized by symptoms such as abdominal pain, bloating, and altered bowel habits. Recent research has focused on the gut microbiota's role in IBS, aiming to identify specific microbial signatures associated with the condition.
Escherichia coli (E. coli)
Escherichia coli (E. coli) is a versatile bacterium, from gut commensal to pathogen, linked to chronic conditions like endometriosis.
Irritable Bowel Syndrome (IBS)
Irritable Bowel Syndrome (IBS) is a common gastrointestinal disorder characterized by symptoms such as abdominal pain, bloating, and altered bowel habits. Recent research has focused on the gut microbiota's role in IBS, aiming to identify specific microbial signatures associated with the condition.
Lactoferrin
Lactoferrin (LF) is a naturally occurring iron-binding glycoprotein classified as a postbiotic with immunomodulatory, antimicrobial, and prebiotic-like properties.
References
- Low nickel diet in dermatology.. Sharma AD.. (Indian J Dermatol. 2013)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Nickel chelation therapy as an approach to combat multi-drug resistant enteric pathogens.. Benoit SL, Schmalstig AA, Glushka J, Maier SE, Edison AS, Maier RJ.. (Sci Rep. 2019.)
- Nickel free-diet enhances the Helicobacter pylori eradication rate: a pilot study.. Campanale M, Nucera E, Ojetti V, Cesario V, Di Rienzo TA, D'Angelo G, Pecere S, Barbaro F, Gigante G, De Pasquale T, Rizzi A, Cammarota G, Schiavino D, Franceschi F, Gasbarrini A.. (Dig Dis Sci. 2014.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Role of Nickel in Microbial Pathogenesis.. Maier RJ, Benoit SL.. (Inorganics. 2019; 7(7):80.)
- Bacterial Exposure to Nickel: Influence on Adhesion and Biofilm Formation on Orthodontic Archwires and Sensitivity to Antimicrobial Agents.. Pavlic A, Begic G, Tota M, Abram M, Spalj S, Gobin I.. (Materials (Basel). 2021.)
- Nickel requirement and factor F430 content of methanogenic bacteria.. Diekert G, Konheiser U, Piechulla K, Thauer RK.. (J Bacteriol. 1981.)
Maier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewMaier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewBenoit SL, Schmalstig AA, Glushka J, Maier SE, Edison AS, Maier RJ.
Nickel chelation therapy as an approach to combat multi-drug resistant enteric pathogens.Sci Rep. 2019.
Read ReviewCampanale M, Nucera E, Ojetti V, Cesario V, Di Rienzo TA, D'Angelo G, Pecere S, Barbaro F, Gigante G, De Pasquale T, Rizzi A, Cammarota G, Schiavino D, Franceschi F, Gasbarrini A.
Nickel free-diet enhances the Helicobacter pylori eradication rate: a pilot study.Dig Dis Sci. 2014.
Maier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewMaier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewMaier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewMaier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewMaier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewMaier RJ, Benoit SL.
Role of Nickel in Microbial Pathogenesis.Inorganics. 2019; 7(7):80.
Read ReviewPavlic A, Begic G, Tota M, Abram M, Spalj S, Gobin I.
Bacterial Exposure to Nickel: Influence on Adhesion and Biofilm Formation on Orthodontic Archwires and Sensitivity to Antimicrobial Agents.Materials (Basel). 2021.
Diekert G, Konheiser U, Piechulla K, Thauer RK.
Nickel requirement and factor F430 content of methanogenic bacteria.J Bacteriol. 1981.