Inflammatory Bowel Disease (IBD)

A colon and coiled small-bowel orientation appears beside two separate layered bowel-wall cutaways with visibly different outer-wall contours. — **Bowel-structure teaching reconstruction** Editorially reviewed
Representative structural-inflammation orientation for inflammatory bowel disease. The selected wall models are not literal endoscopy or histology and cannot classify Crohn disease or ulcerative colitis, stage, severity, complication, or diagnosis.
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Inflammatory Bowel Diseasescondition
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MeSH:D015212
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Inflammatory Bowel Diseases — MeSH Definition & Facts for Crohn's Disease
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CC BY-SA 4.0Created 2026-09-06

An umbrella term for chronic relapsing-remitting inflammatory conditions of the gastrointestinal tract, principally Crohn's Disease (CD; transmural, any GI segment) and ulcerative colitis (UC; mucosal, colon only). Approximately 6 million patients worldwide.

IBD represents the most direct manifestation of gut Dysbiosis, barrier failure, and immune dysregulation—the same triad that metals produce—making it a central disease in the Metallomics-microbiome framework.

Evidence map30 cited passagesInspect provenance +

Zinc Depletion

The ZIP8 (SLC39A8) A391T variant in Crohn's disease directly links zinc transport dysfunction to barrier integrity, microbiome composition, and inflammation.

Selenium and Other Trace Elements

Selenium significantly lower in both CD and UC vs controls; impairs selenoprotein-dependent antioxidant defense (GPx, TrxR).

Selenium and Other Trace Elements

Manganese depleted in UC patients. Nickel elevated in active CD vs inactive UC.

Selenium and Other Trace Elements

Thallium positively associated with UC disease activity—a novel finding.

IBD-CVD Comorbidity

Shared mechanisms: chronic inflammation, endothelial dysfunction, tmao elevation, dysbiosis-driven LPS translocation.

Iron Dysregulation

Iron deficiency anemia affects 36-76% of IBD patients, driven by chronic blood loss, malabsorption, and inflammation-mediated iron sequestration (, cross-sectional, n=153). hepcidin is elevated by IL-6 during IBD flares, blocking ferroportin-mediated iron export from enterocytes and macrophages—trapping iron intracellularly while producing systemic defici

Iron Dysregulation

The oral iron paradox: Supplementation worsens dysbiosis by providing growth substrate for siderophilic pathogens (Enterobacteriaceae, E. coli) while suppressing beneficial anaerobes (; ).

Zinc Depletion

Zinc is depleted via diarrheal losses, malabsorption, and increased urinary excretion during inflammation. Depletion impairs intestinal barrier integrity (ZO-1, claudin-1 expression), wound healing, and immune function. The ZIP8 A391T variant in Crohn's disease directly links zinc transport dysfunction to barrier integrity, microbiome composition, and inflam

Selenium and Trace Element Depletion

Selenium is significantly lower in both CD and UC versus controls, impairing selenoprotein-dependent antioxidant defense (GPx, TrxR) (). Manganese is depleted in UC patients. Nickel is elevated in active CD versus inactive UC. Thallium is positively associated with UC disease activity—a novel finding ().

Copper Elevation

copper is positively associated with CRP in CD (), consistent with ceruloplasmin elevation during the acute-phase response. Copper elevation supports oxidative stress through Fenton-like chemistry while simultaneously being deployed by macrophages as an antimicrobial weapon.

Environmental Exposures

NSAIDs: Induce enteropathy and alter gut microbiome composition, compounding barrier dysfunction (; )

Environmental Exposures

Antibiotics: Usage within 1 month increases microbial dysbiosis index independent of genetic effects ()

Environmental Exposures

Dietary patterns: Mediterranean diet is protective against CD (HR: 0.42) but not UC ()

Nutritional Immunity Response

calprotectin—The gold-standard non-invasive IBD biomarker. S100A8/A9 protein released by activated neutrophils; sequesters zinc and manganese from pathogens. Fecal calprotectin correlates with endoscopic disease activity and is simultaneously a diagnostic marker and an active nutritional immunity agent ().

Enriched Taxa

escherichia coli and enterobacteriaceae—The hallmark IBD bloom. AIEC in CD (75% prevalence in ileal mucosa vs 6% healthy ()); Enterobacteriaceae expansion associated with NOD2 risk allele dosage (). These organisms thrive via siderophore-mediated iron acquisition in the inflamed, iron-rich mucosal environment.

Enriched Taxa

fusobacterium nucleatum—Pro-inflammatory; adhesin-mediated mucosal colonization; NF-kB activation. Enriched in both CD and colorectal cancer ().

Depleted Taxa

faecalibacterium prausnitzii—The most consistently depleted taxon across all IBD cohorts (; ). Primary butyrate producer; suppresses NF-kB and induces IL-10. Its depletion is the single most informative taxonomic biomarker for IBD.

Depleted Taxa

lachnospiraceae family—Mendelian randomization confirms causal protective role: Lachnospiraceae UCG001 protective for CD (OR: 0.81); Eubacterium ventriosum protective for UC (OR: 0.68) (, computational prediction).

Depleted Taxa

Firmicutes/Bacteroidetes ratio is consistently altered in IBD, with reduced microbial diversity overall ().

Ecological State

Barrier dysfunction—Tight junction degradation (zinc-dependent claudins/occludins impaired by zinc depletion; E-cadherin cleaved by BFT toxin); reduced mucus layer thickness (mucinase activity from R. gnavus); impaired Paneth cell defensin secretion (NOD2 mutations + zinc depletion) ().

Ecological State

Ferroptosis—Intracellular iron trapping during hepcidin elevation catalyzes lipid peroxidation through Fenton chemistry. GPX3 is causally protective ().

Ecological State

LPS translocation—Bacterial translocation across the compromised epithelium triggers innate immune activation via NF-kB; systemic LPS absorption drives endothelial dysfunction and CVD risk ().

Ecological State

TMAO elevation—Dysbiosis-driven trimethylamine N-oxide production promotes foam cell formation, endothelial dysfunction, and platelet activation—linking IBD to cardiovascular disease risk (, expert opinion).

[[crohns-disease]] (overlap score: 0.90) and [[ulcerative-colitis]] (overlap score: 0.88)

As IBD subtypes, CD and UC share the core signature but differ in important ways. CD shows more severe alpha diversity reduction (). Mediterranean diet protects against CD but not UC. Mendelian randomization reveals disease-specific causal genera (). Metal profiles differ: thallium associates with UC activity while copper-CRP association is CD-specific ().

Showing 24 of 30 evidence-bearing passages. Every remaining citation is still indexed in the reference record below.

Integrated microbiome signature

One disease. Five evidence layers.

A generated systems view of the metals, organisms, host sequestration signals, ecological conditions, and microbial functions indexed for Inflammatory Bowel Disease (IBD).

Evidence layer

Metallomic signature

Elements and antioxidants reported as elevated, accumulated, depleted, or systemically altered.

high confidence

↑

Elevated or accumulated

Iron MucosalCopper

↓

Depleted or redistributed

Iron SystemicZinc Selenium Manganese Glutathione (GSH)

Evidence layer

Taxonomic signature

Organisms reported as enriched or depleted, with their indexed functional context kept beside the name.

high confidence

Enriched taxa4

Escherichia coli

AIEC in CD; enterotoxigenic strains in UC; siderophore-dependent iron acquisition; LPS/TLR4/NF-kB activation; Enterobacteriaceae bloom is hallmark of IBD

Fusobacterium nucleatum

Pro-inflammatory; NF-kB activation; adhesin-mediated mucosal colonization; enriched in both CD and CRC

Ruminococcus gnavus

Mucin-degrading; barrier damage; enriched across IBD subtypes

Enterobacteriaceae

Bloom favored by inflammation-driven iron redistribution and oxygen availability; NOD2 allele dosage-dependent

Depleted taxa6

Faecalibacterium prausnitzii

Primary butyrate producer; anti-inflammatory (NF-kB suppression, IL-10 induction); most consistently depleted taxon in IBD across all cohorts

Roseburia

Butyrate and propionate producer; part of Clostridia cluster XIVa; consistently reduced in IBD

Blautia

SCFA production; depleted in IBD; contributes to butyrate collapse

Bifidobacterium

Carbohydrate fermentation and cross-feeding with butyrate producers; depleted in IBD

Lachnospiraceae (Family)

SCFA production; Mendelian randomization confirms causal protective role in IBD and CD specifically

Prevotella

Depleted in IBD; associated with plant-rich dietary patterns

Evidence layer

Nutritional immunity

Host metal-withholding, inflammatory, antioxidant, and microbial-metabolite signals indexed in the signature.

high confidence

↑

Elevated host signals

Calprotectin (S100A8/A9)Hepcidin Lactoferrin Lipocalin-2

↓

Depleted protective signals

Glutathione (GSH)Alpha Defensins

Evidence layer

Ecological state

The environmental conditions that connect the organism-level observations into a system.

high confidence

WB.ECO / SYSTEM MODEL6 connected states

Butyrate Collapseindexed ecological state

Barrier Dysfunctionindexed ecological state

Ferroptosisindexed ecological state

Firmicutes Bacteroidetes Ratio Shiftindexed ecological state

LPS Translocationindexed ecological state

TMAO Elevationindexed ecological state

Evidence layer

Virulence functions

Microbial structures, enzymes, and acquisition systems implicated by the linked evidence.

moderate confidence

SiderophoresFimH AdhesinOuter Membrane VesiclesZinc Metalloprotease BFTMucinase

Encyclopedia article

The disease record, in full.

The original WikiBiome disease narrative remains intact beneath the generated signature atlas.

Metallomic Signature#

Iron Dysregulation: The Defining Metal Feature#

Iron deficiency anemia affects 36-76% of IBD patients, driven by chronic blood loss, malabsorption, and Metal-Driven Inflammation-mediated iron sequestration.

Hepcidin is elevated by IL-6 during IBD flares, blocking ferroportin-mediated iron export from enterocytes and macrophages—trapping iron intracellularly while producing systemic deficiency.

This creates a paradox: intracellular iron excess (promoting Oxidative Stress and potentially Ferroptosis) alongside systemic iron deficiency (causing anemia and fatigue). Oral iron supplementation worsens dysbiosis by providing growth substrate for siderophilic pathogens (Enterobacteriaceae, E. coli) while suppressing beneficial anaerobes.

Zinc Depletion#

Zinc is depleted in IBD via diarrheal losses, malabsorption, and increased urinary excretion during inflammation. zinc (Zn) deficiency impairs intestinal barrier integrity (ZO-1, claudin-1 expression), wound healing, and immune function.

The ZIP8 (SLC39A8) A391T variant in Crohn's disease directly links zinc transport dysfunction to barrier integrity, microbiome composition, and inflammation.^{[1]ZIP8 A391T Crohn's Disease-Linked Risk Variant Induces Colonic Metal Ion Dyshomeostasis, Microbiome Compositional Shifts, and InflammationYang JC, Zhao M, Chernikova D et al. · 2024Open reference 1 ↓}

Selenium and Other Trace Elements#

Selenium significantly lower in both CD and UC vs controls; impairs selenoprotein-dependent antioxidant defense (GPx, TrxR).^{[2]Clinical and inflammatory biomarkers of inflammatory bowel diseases are linked to plasma trace elements and toxic metals; new insights into an old conceptAmerikanou C, Karavoltsos S, Gioxari A et al. · 2022Open reference 2 ↓} Manganese depleted in UC patients. Nickel elevated in active CD vs inactive UC.^{[2]Clinical and inflammatory biomarkers of inflammatory bowel diseases are linked to plasma trace elements and toxic metals; new insights into an old conceptAmerikanou C, Karavoltsos S, Gioxari A et al. · 2022Open reference 2 ↓}

Thallium positively associated with UC disease activity—a novel finding.^{[2]Clinical and inflammatory biomarkers of inflammatory bowel diseases are linked to plasma trace elements and toxic metals; new insights into an old conceptAmerikanou C, Karavoltsos S, Gioxari A et al. · 2022Open reference 2 ↓}

Dysbiosis Signature#

IBD dysbiosis is among the most characterized in the literature. Depleted: Faecalibacterium prausnitzii (most consistent finding), Roseburia, Blautia, Bifidobacterium, Prevotella—all major Short-Chain Fatty Acids (SCFAs) producers. Enriched: Enterobacteriaceae (adherent-invasive E. coli in CD), Fusobacterium, Ruminococcus gnavus.

Firmicutes/Bacteroidetes ratio altered; reduced microbial diversity overall.

This signature overlaps substantially with metal-induced dysbiosis patterns, raising the question of whether environmental metal exposure contributes to IBD incidence.

Biomarkers#

Fecal Calprotectin (S100A8/A9): The gold-standard non-invasive biomarker for intestinal inflammation in IBD. S100A8/A9 protein released by activated neutrophils; sequesters zinc and manganese as part of Nutritional Immunity (Metal Sequestration). Correlates with endoscopic disease activity.

CRP, SAA: Systemic inflammation markers; CRP elevated in active disease. Fecal lactoferrin: Iron-binding neutrophil protein; elevated in active IBD. IL-6, TNF-alpha, IL-1beta: Pro-inflammatory cytokines driving disease pathology.

IBD-CVD Comorbidity#

IBD patients have significantly increased Cardiovascular Disease risk.

2x increased heart failure risk; 19% increase in HF risk up to 20 years post-diagnosis. Shared mechanisms: chronic inflammation, endothelial dysfunction, Trimethylamine N-Oxide (TMAO) elevation, dysbiosis-driven LPS translocation.^{[3]Inflammatory Bowel Disease and Cardiovascular Disease: An Integrative Review With a Focus on the Gut MicrobiomeCamila Sanchez Cruz, Anahi Rojas Huerta, Jesus Lima Barrientos et al. · 2024Open reference 3 ↓} Calprotectin (S100A8/A9) and CRP predict both IBD activity and CVD risk.

Connections#

Crohn's Disease—transmural IBD subtype; ZIP8 variant links metal transport to pathogenesis
Calprotectin (S100A8/A9)—gold-standard IBD biomarker; metal-sequestering antimicrobial protein
Hepcidin—iron-regulatory hormone elevated in IBD, driving the anemia-of-inflammation paradox
Ferroptosis—intracellular iron trapping during hepcidin elevation may promote ferroptotic cell death
Short-Chain Fatty Acids (SCFAs)—SCFA producer depletion is the functional consequence of IBD dysbiosis
dysbiosis—IBD has the most characterized dysbiosis signature in the literature
inflammation—chronic NF-kB-driven inflammation is the hallmark of IBD
Cardiovascular Disease—IBD patients at significantly increased CVD risk via shared inflammatory mechanisms
Nutritional Immunity (Metal Sequestration)—calprotectin and lactoferrin are nutritional immunity effectors elevated in IBD
Metal-Disease Matrix: A Cross-Source Synthesis—IBD is a key disease in the metal-disease interaction landscape
Prebiotics—prebiotic fiber supports SCFA producer recovery in IBD remission maintenance
Fecal Microbiota Transplant (FMT)—strongest evidence in UC subtype; 25-35% remission; donor diversity predicts response
Microbial Biomarkers—fecal calprotectin and microbial diversity as non-invasive IBD monitoring tools
Microbiome-Derived Metabolites—SCFA depletion, bile acid alterations, and tryptophan shunting in IBD
Biomarkers—calprotectin, CRP, hepcidin, and metallomic panels for disease activity tracking

Generated evidence record

References 19

Numbered by first appearance in the article, then reconciled with its declared source list.

1
★Yang JC, Zhao M, Chernikova D et al. (2024). ZIP8 A391T Crohn's Disease-Linked Risk Variant Induces Colonic Metal Ion Dyshomeostasis, Microbiome Compositional Shifts, and Inflammation. Digestive Diseases and Sciences.
WikiBiome source record Are you an author?doi:10.3389/fimmu.2023.1183914
2
Amerikanou C, Karavoltsos S, Gioxari A et al. (2022). Clinical and inflammatory biomarkers of inflammatory bowel diseases are linked to plasma trace elements and toxic metals; new insights into an old concept. Frontiers in Nutrition.
WikiBiome source record Are you an author?doi:10.3389/fnut.2022.997356
3
Camila Sanchez Cruz, Anahi Rojas Huerta, Jesus Lima Barrientos et al. (2024). Inflammatory Bowel Disease and Cardiovascular Disease: An Integrative Review With a Focus on the Gut Microbiome. Cureus.
WikiBiome source record Are you an author?doi:10.7759/cureus.65136
4
Zhu R, He P, Liu Z et al. (2021). Editorial: Microbiome in IBD: From Composition to Therapy. Frontiers in Pharmacology.
WikiBiome source record Are you an author?doi:10.3389/fphar.2021.721992
5
Rashed R, Valcheva R, Dieleman LA (2022). Manipulation of Gut Microbiota as a Key Target for Crohn's Disease. Frontiers in Medicine.
WikiBiome source record Are you an author?doi:10.3389/fmed.2022.887044
6
Borghini R, Porpora MG, Casale R et al. (2020). Irritable Bowel Syndrome-Like Disorders in Endometriosis: Prevalence of Nickel Sensitivity and Effects of a Low-Nickel Diet. An Open-Label Pilot Study. Nutrients.
WikiBiome source record Are you an author?doi:10.3390/nu12082277
7
Syer SD, Blackler RW, Martin R et al. (2015). NSAID Enteropathy and Bacteria: A Complicated Relationship. Journal of Gastroenterology.
WikiBiome source record Are you an author?doi:10.1007/s00535-014-1032-1
8
Fabian Mermans, Evelien Heiremans, Maud Van Belleghem et al. (2019). Nonsteroidal Anti-Inflammatory Drugs as Therapeutic Allies of the Gut Microbiome on Chronic Inflammation. Facta Universitatis Series Medicine and Biology.
WikiBiome source record Are you an author?doi:10.22190/FUMB201222013M
9
Li H, Christman LM, Li R et al. (2020). Synergic Interactions between Polyphenols and Gut Microbiota in Mitigating Inflammatory Bowel Diseases. Food & Function.
WikiBiome source record Are you an author?doi:10.1039/D0FO00713G
10
Knights D, Silverberg MS, Weersma RK et al. (2014). Complex Host Genetics Influence the Microbiome in Inflammatory Bowel Disease. Genome Medicine.
WikiBiome source record Are you an author?doi:10.1186/s13073-014-0107-1
11
Khalili H, Hakansson N, Chan SS et al. (2024). Adherence to a Mediterranean Diet is Associated with a Lower Risk of Later-Onset Crohn's Disease: Results From Two Large Prospective Cohort Studies. Gut.
WikiBiome source record Are you an author?doi:10.1136/gutjnl-2023-331587
12
Haag LM, Siegmund B (2015). Intestinal Microbiota and the Innate Immune System - a Crosstalk in Crohn's Disease Pathogenesis. Frontiers in Immunology.
WikiBiome source record Are you an author?doi:10.3389/fimmu.2015.00489
13
Kang DY, Park JL, Yeo MK et al. (2023). Diagnosis of Crohn's Disease and Ulcerative Colitis Using the Microbiome. BMC Microbiology.
WikiBiome source record Are you an author?doi:10.1186/s12866-023-03084-5
14
Liu B, Ye D, Yang H et al. (2022). Two-Sample Mendelian Randomization Analysis Investigates Causal Associations Between Gut Microbial Genera and Inflammatory Bowel Disease, and Specificity Causal Associations in Ulcerative Colitis or Crohn's Disease. Frontiers in Immunology.
WikiBiome source record Are you an author?doi:10.3389/fimmu.2022.921546
15
Xu S, Li X, Zhang S et al. (2023). Oxidative Stress Gene Expression, DNA Methylation, and Gut Microbiota Interaction Trigger Crohn's Disease: a Multi-Omics Mendelian Randomization Study. BMC Medicine.
WikiBiome source record Are you an author?doi:10.1186/s12916-023-02878-8
16
Shen J, Zuo ZX, Mao AP (2014). Effect of Probiotics on Inducing Remission and Maintaining Therapy in Ulcerative Colitis, Crohn's Disease, and Pouchitis: Meta-analysis of Randomized Controlled Trials. Inflammatory Bowel Diseases.
WikiBiome source record Are you an author?doi:10.1097/01.MIB.0000437495.30052.be
17
Li P, Zhang T, Xiao Y et al. (2019). Timing for the Second Fecal Microbiota Transplantation to Maintain the Long-Term Benefit from the First Treatment for Crohn's Disease. Applied Microbiology and Biotechnology.
WikiBiome source record Are you an author?doi:10.1007/s00253-018-9447-x
18
Sokol H, Landman C, Seksik P et al. (2020). Fecal Microbiota Transplantation to Maintain Remission in Crohn's Disease: A Pilot Randomized Controlled Study. Microbiome.
WikiBiome source record Are you an author?doi:10.1186/s40168-020-0792-5
19
Zhang M, Sun K, Wu Y et al. (2017). Interactions between Intestinal Microbiota and Host Immune Response in Inflammatory Bowel Disease. Frontiers in Immunology.
WikiBiome source record Are you an author?doi:10.3389/fimmu.2017.00942

Knowledge graph

Article network

Current recordInflammatory Bowel Disease (IBD)Diseases

Mentioned here 18

Crohn's Disease Dysbiosis Metallomics Metal-Driven Inflammation Hepcidin Oxidative Stress Ferroptosis Faecalibacterium prausnitzii Blautia Bifidobacterium Short-Chain Fatty Acids (SCFAs)Calprotectin (S100A8/A9)Nutritional Immunity (Metal Sequestration)Cardiovascular Disease Trimethylamine N-Oxide (TMAO)Metal-Disease Matrix: A Cross-Source Synthesis Prebiotics Fecal Microbiota Transplant (FMT)

Pages linking here 47

Bacteroides thetaiotaomicron Bilophila Celiac Disease Colorectal Cancer Depression Endometriosis Fusicatenibacter Fusobacterium nucleatum Fusobacterium varium Holdemanella Irritable Bowel Syndrome (IBS)Lactococcus Morganella morganii Multiple Sclerosis Odoribacter Olsenella Oscillospiraceae Parabacteroides distasonis

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MetalsIronRead article →MechanismsButyrateRead article →MetalsZincRead article →DiseasesColorectal CancerRead article →DiseasesUlcerative ColitisRead article →MicroorganismsLachnospiraceaeRead article →

Metallomic Signature#

Iron Dysregulation: The Defining Metal Feature#

Zinc Depletion#

Selenium and Other Trace Elements#

Dysbiosis Signature#

Biomarkers#

IBD-CVD Comorbidity#

Connections#

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Strengthen Metallomics and link high-leverage contexts

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