Component
Granulocyte-macrophage colony-stimulating factor / GM-CSF
Granulocyte-macrophage colony-stimulating factor / GM-CSF. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Where it participates (unsigned role)
Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"}
- experimental_model
- Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models
- exposure
- Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy
- limitations
- A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Mouse
- plain_language
- The change is not only in the cells circulating now; it reaches the factory that makes the next ones.
- primary_references
- [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
- tissue_or_cell_type
- Bone marrow
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models · source_derived_draft · unverified_draft
### bg-training-reaches-the-marrow Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The change is not only in the cells circulating now; it reaches the factory that makes the next ones. organism: Mouse tissue_or_cell_type: Bone marrow experimental_model: Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models limitations: A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow. exposure: Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy evidence_span: {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"} [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.