Component

Human interleukin-8 / CXCL8

Context-specific entity; species, compartment and exposure are stated on each claim.

10 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. In 37 colorectal-cancer patients receiving chemotherapy, 100 mg/day fisetin for seven weeks lowered plasma IL-8 relative to placebo.

    Fisetin → Human interleukin-8 / CXCL8 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Randomized double-blind trial; 18 fisetin and 19 placebo.
    limitations
    No tumor-response or survival benefit demonstrated; plasma concentration is not direct cytokine binding.
    nutrient_topic
    Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin
    plain_language
    A small trial measured an inflammatory marker response.
    primary_references
    Effect of fisetin supplementation on inflammatory factors and matrix metalloproteinase enzymes in colorectal cancer patients. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29541713/ · DOI 10.1039/c7fo01898c
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 504–510

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized double-blind trial; 18 fisetin and 19 placebo. · source_derived_draft · unverified_draft

    ## fisetin-crc-il8 A small trial measured an inflammatory marker response. In 37 colorectal-cancer patients receiving chemotherapy, 100 mg/day fisetin for seven weeks lowered plasma IL-8 relative to placebo. Model: Randomized double-blind trial; 18 fisetin and 19 placebo. Limitations: No tumor-response or survival benefit demonstrated; plasma concentration is not direct cytokine binding. Evidence access: Primary abstract Effect of fisetin supplementation on inflammatory factors and matrix metalloproteinase enzymes in colorectal cancer patients. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29541713/ · DOI 10.1039/c7fo01898c
    Complete structured claim and evidence

  2. Astaxanthin reduced H. pylori-induced ROS, NF-kappa-B activation and IL-8 expression in human AGS cells.

    Astaxanthin → Human interleukin-8 / CXCL8 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human gastric adenocarcinoma cell line, H. pylori challenge.
    limitations
    Not a clinical eradication trial and not proof of identical behavior in normal gastric tissue.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    The challenged gastric cells produced a smaller inflammatory signal.
    primary_references
    Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 294–300

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human gastric adenocarcinoma cell line, H. pylori challenge. · source_derived_draft · unverified_draft

    ## astaxanthin-gastric-il8 The challenged gastric cells produced a smaller inflammatory signal. Astaxanthin reduced H. pylori-induced ROS, NF-kappa-B activation and IL-8 expression in human AGS cells. Model: Human gastric adenocarcinoma cell line, H. pylori challenge. Limitations: Not a clinical eradication trial and not proof of identical behavior in normal gastric tissue. Evidence access: Primary abstract Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
    Complete structured claim and evidence

  3. All-E, 9Z and 13Z astaxanthin at 1.2 micromolar reduced TNF-induced IL-8 secretion by 22–27% in Caco-2 cells, with reduced I-kappa-B-alpha phosphorylation.

    Astaxanthin → Human interleukin-8 / CXCL8 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human Caco-2 monolayers with TNF challenge.
    limitations
    Different isomer responses do not establish a preferred clinical formulation.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    The absorbed forms also changed inflammatory signaling in intestinal cells.
    primary_references
    Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 486–492

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 monolayers with TNF challenge. · source_derived_draft · unverified_draft

    ## astaxanthin-intestinal-inflammatory-signal The absorbed forms also changed inflammatory signaling in intestinal cells. All-E, 9Z and 13Z astaxanthin at 1.2 micromolar reduced TNF-induced IL-8 secretion by 22–27% in Caco-2 cells, with reduced I-kappa-B-alpha phosphorylation. Model: Human Caco-2 monolayers with TNF challenge. Limitations: Different isomer responses do not establish a preferred clinical formulation. Evidence access: Primary abstract Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Expression of endothelial nitric oxide synthase and nitrite concentrations were significantly increased in treated subjects, and treatment sensitised macrophages to release FGF-2 and EGF while increasing the neutrophil attractant CXCL-8 and thereby the release of CCL2.

    Hyperbaric oxygen therapy → Nitrite concentration in wound tissue source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"}
    experimental_model
    Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies
    exposure
    Hyperbaric oxygen with standard wound care for 20 days
    limitations
    A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue.
    nutrient_topic
    Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy
    organism
    Human
    plain_language
    The same nitric oxide enzyme appears again, this time in the wound, with the immune cells joining in.
    primary_references
    [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031
    tissue_or_cell_type
    Diabetic foot ulcer tissue

    Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 842–853

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies · source_derived_draft · unverified_draft

    ### hbot-enos-nitrite-wound Expression of endothelial nitric oxide synthase and nitrite concentrations were significantly increased in treated subjects, and treatment sensitised macrophages to release FGF-2 and EGF while increasing the neutrophil attractant CXCL-8 and thereby the release of CCL2. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The same nitric oxide enzyme appears again, this time in the wound, with the immune cells joining in. organism: Human tissue_or_cell_type: Diabetic foot ulcer tissue experimental_model: Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies limitations: A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue. exposure: Hyperbaric oxygen with standard wound care for 20 days evidence_span: {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"} [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031
    Complete structured claim and evidence

  2. Bromelain removed CXCR1/CXCR2 from human neutrophils and reduced IL-8-directed migration by about 40%.

    Bromelain → Human CXCR1/CXCR2 chemokine receptors source_derived_draftungraded
    Experimental context and source evidence
    dose
    In-vitro bromelain treatment; in-vivo preparation specified in the primary study
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Isolated human neutrophils; three murine inflammation models
    limitations
    The effect was stimulus-selective and does not imply global suppression of neutrophil migration or human clinical efficacy.
    nutrient_topic
    Bromelain chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Bromelain
    organism
    Isolated human neutrophils; three murine inflammation models
    plain_language
    Bromelain removed CXCR1/CXCR2 from human neutrophils and reduced IL-8-directed migration by about 40%.
    primary_references
    Bromelain treatment decreases neutrophil migration to sites of inflammation. (2008). https://pubmed.ncbi.nlm.nih.gov/18482869/ DOI: 10.1016/j.clim.2008.02.015
    route
    In vitro and in vivo
    tissue
    Chemokine-receptor surface expression and chemotaxis

    Bromelain: mechanism of action and interactions (2026-09-20) · lines 33–42

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Isolated human neutrophils; three murine inflammation models · source_derived_draft · unverified_draft

    ## bromelain-neutrophil-cxcr Bromelain removed CXCR1/CXCR2 from human neutrophils and reduced IL-8-directed migration by about 40%. Model/species: Isolated human neutrophils; three murine inflammation models Tissue/system: Chemokine-receptor surface expression and chemotaxis Exposure: In-vitro bromelain treatment; in-vivo preparation specified in the primary study Route: In vitro and in vivo Duration: Acute Limits: The effect was stimulus-selective and does not imply global suppression of neutrophil migration or human clinical efficacy. Primary reference: Bromelain treatment decreases neutrophil migration to sites of inflammation. (2008). https://pubmed.ncbi.nlm.nih.gov/18482869/ DOI: 10.1016/j.clim.2008.02.015 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. Reference fulvic fractions increased IL-6 and IL-8 release from respiratory epithelial cells.

    Suwannee River fulvic acid reference material → IL6 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions.
    limitations
    Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial.
    nutrient_topic
    Fulvic acid collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Fulvic acid (heterogeneous humic fraction)
    plain_language
    Direct airway-cell exposure stimulated inflammatory mediators.
    primary_references
    A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036

    Fulvic acid: mixture identity, mineral chemistry, signaling and cross-nutrient mechanisms (2026-09-19) · lines 220–226

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. · source_derived_draft · unverified_draft

    ## fulvic-acid-airway-inflammation Direct airway-cell exposure stimulated inflammatory mediators. Reference fulvic fractions increased IL-6 and IL-8 release from respiratory epithelial cells. Model: Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. Limitations: Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial. Evidence access: Primary abstract A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036
    Complete structured claim and evidence

  4. Iron co-exposure reduced fulvic-associated IL-6/IL-8 release in the tested cells.

    Iron → Cytokine release after reference fulvic exposure in airway cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions.
    limitations
    Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial. This is not a recommendation to supplement iron or proof of systemic iron deficiency.
    nutrient_topic
    Fulvic acid collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Fulvic acid (heterogeneous humic fraction)
    plain_language
    Adding iron altered the inflammatory response in this experiment.
    primary_references
    A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036

    Fulvic acid: mixture identity, mineral chemistry, signaling and cross-nutrient mechanisms (2026-09-19) · lines 228–234

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. · source_derived_draft · unverified_draft

    ## fulvic-acid-airway-iron-rescue Adding iron altered the inflammatory response in this experiment. Iron co-exposure reduced fulvic-associated IL-6/IL-8 release in the tested cells. Model: Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. Limitations: Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial. This is not a recommendation to supplement iron or proof of systemic iron deficiency. Evidence access: Primary abstract A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036
    Complete structured claim and evidence

  5. Astaxanthin increased PPAR-gamma and catalase expression in challenged AGS cells; the PPAR-gamma antagonist GW9662 suppressed the ROS/IL-8 protective response.

    Astaxanthin → Human catalase / CAT source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human AGS expression assays and pharmacological inhibition.
    limitations
    Antagonist sensitivity is not direct binding evidence or a demonstration of iron deficiency rescue.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    A receptor-linked antioxidant enzyme response contributed in this model.
    primary_references
    Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 302–308

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human AGS expression assays and pharmacological inhibition. · source_derived_draft · unverified_draft

    ## astaxanthin-gastric-catalase A receptor-linked antioxidant enzyme response contributed in this model. Astaxanthin increased PPAR-gamma and catalase expression in challenged AGS cells; the PPAR-gamma antagonist GW9662 suppressed the ROS/IL-8 protective response. Model: Human AGS expression assays and pharmacological inhibition. Limitations: Antagonist sensitivity is not direct binding evidence or a demonstration of iron deficiency rescue. Evidence access: Primary abstract Astaxanthin Inhibits Mitochondrial Dysfunction and Interleukin-8 Expression in Helicobacter pylori-Infected Gastric Epithelial Cells. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30231525/ · DOI 10.3390/nu10091320
    Complete structured claim and evidence

  6. CLA treatment increased IL-6 and IL-8 secretion from the human adipose culture systems.

    trans-10,cis-12 conjugated linoleic acid → Human adipocyte CLA-associated cytokine output source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human adipocytes, stromal-vascular cells and adipose explants.
    limitations
    Culture concentrations and cell mixtures limit extrapolation.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    The response could signal to neighboring cells.
    primary_references
    Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 134–140

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocytes, stromal-vascular cells and adipose explants. · source_derived_draft · unverified_draft

    ## cla-cytokines The response could signal to neighboring cells. CLA treatment increased IL-6 and IL-8 secretion from the human adipose culture systems. Model: Human adipocytes, stromal-vascular cells and adipose explants. Limitations: Culture concentrations and cell mixtures limit extrapolation. Evidence access: Primary abstract Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
    Complete structured claim and evidence

  7. DGK-eta siRNA reduced CLA-induced IL-8 and MCP-1 expression and JNK/c-Jun activation.

    Human diacylglycerol kinase eta / DGKH → Human adipocyte CLA-associated cytokine output source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human adipocyte RNA-interference experiment.
    limitations
    Partial effects do not establish an exclusive pathway.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Gene depletion supported a contribution by a specific enzyme.
    primary_references
    Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 190–196

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte RNA-interference experiment. · source_derived_draft · unverified_draft

    ## cla-dgkh-knockdown Gene depletion supported a contribution by a specific enzyme. DGK-eta siRNA reduced CLA-induced IL-8 and MCP-1 expression and JNK/c-Jun activation. Model: Human adipocyte RNA-interference experiment. Limitations: Partial effects do not establish an exclusive pathway. Evidence access: Primary abstract Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards