Candida albicans

Where it participates (unsigned role)

1. All four affected family members had a homozygous point mutation in CARD9 resulting in a premature termination codon Q295X, healthy family members had wild-type expression of the CARD9 protein while the four patients lacked wild-type expression which was associated with low numbers of interleukin-17-producing helper T cells, and functional studies based on genetic reconstitution of myeloid cells from Card9-null mice showed that the Q295X mutation impairs innate signalling from the antifungal pattern-recognition receptor dectin-1.

   The homozygous CARD9 Q295X premature termination variant → Dectin-1 / CLEC7A source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   machinery_impairment Imported condition classification; unverified.

   evidence_span

   {"source_cache": "artifacts/glucan-research/19864672.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3", "start_char": 0, "end_char": 1842, "text_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3"}

   experimental_model

   Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled

   exposure

   Naturally occurring homozygous CARD9 Q295X premature termination, with reconstitution in Card9-null mouse myeloid cells

   limitations

   Human genetics with a linkage score of 3.6 and functional confirmation. It establishes the importance of the pathway in host defence; it says nothing about beta-glucan as a supplement.

   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

   Human

   plain_language

   People born without this one signalling protein get persistent fungal infections, which is how much the pathway matters.

   primary_references

   [bg-p19864672] A homozygous CARD9 mutation in a family with susceptibility to fungal infections. (2009). https://pubmed.ncbi.nlm.nih.gov/19864672/ DOI: 10.1056/nejmoa0810719

   tissue_or_cell_type

   Leukocytes

   trigger_kind

   machinery_impairment Imported condition classification; unverified.

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 411–422

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled · source_derived_draft · unverified_draft

   ### bg-losing-card9-costs-antifungal-defence All four affected family members had a homozygous point mutation in CARD9 resulting in a premature termination codon Q295X, healthy family members had wild-type expression of the CARD9 protein while the four patients lacked wild-type expression which was associated with low numbers of interleukin-17-producing helper T cells, and functional studies based on genetic reconstitution of myeloid cells from Card9-null mice showed that the Q295X mutation impairs innate signalling from the antifungal pattern-recognition receptor dectin-1. Condition category: machinery_impairment 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: People born without this one signalling protein get persistent fungal infections, which is how much the pathway matters. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled limitations: Human genetics with a linkage score of 3.6 and functional confirmation. It establishes the importance of the pathway in host defence; it says nothing about beta-glucan as a supplement. exposure: Naturally occurring homozygous CARD9 Q295X premature termination, with reconstitution in Card9-null mouse myeloid cells evidence_span: {"source_cache": "artifacts/glucan-research/19864672.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3", "start_char": 0, "end_char": 1842, "text_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3"} [bg-p19864672] A homozygous CARD9 mutation in a family with susceptibility to fungal infections. (2009). https://pubmed.ncbi.nlm.nih.gov/19864672/ DOI: 10.1056/nejmoa0810719

   Complete structured claim and evidence

2. Maximum plasma concentrations for glucan phosphate occurred at 4 hours while laminarin and scleroglucan showed two plasma peaks between 0.5 and 12 hours, at 24 hours 27 plus or minus 3% of the glucan phosphate and 20 plus or minus 7% of the laminarin remained in the serum, following oral administration glucans were bound and internalized by intestinal epithelial cells and gut-associated lymphoid tissue cells with internalization by intestinal epithelial cells not being Dectin-dependent, gut-associated lymphoid tissue expression of Dectin-1 and Toll-like receptor 2 but not Toll-like receptor 4 increased, oral glucan increased systemic levels of interleukin-12 by 151%, and oral glucan administration also increased survival in mice challenged with Staphylococcus aureus or Candida albicans.

   Glucan phosphate → Serum beta-glucan concentration after oral dosing source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glucan-research/15976018.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18", "start_char": 0, "end_char": 1617, "text_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18"}

   experimental_model

   Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice

   exposure

   Glucan phosphate, laminarin and scleroglucan at 1 milligram per kilogram orally in rats, and 1 milligram orally in mice

   limitations

   Rodent pharmacokinetics and rodent challenge models. The reported figure for glucan phosphate at 24 hours is a percentage remaining in serum whose denominator the abstract does not state, so it is not read here as a fraction of the swallowed dose.

   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

   Rat and mouse

   plain_language

   In rodents the swallowed sugar does cross into the circulation, is taken up by the gut immune tissue, and leaves the animals better able to survive an infection.

   primary_references

   [bg-p15976018] Oral delivery and gastrointestinal absorption of soluble glucans stimulate increased resistance to infectious challenge. (2005). https://pubmed.ncbi.nlm.nih.gov/15976018/ DOI: 10.1124/jpet.105.085415

   tissue_or_cell_type

   Plasma, intestinal epithelium and gut-associated lymphoid tissue

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 372–383

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice · source_derived_draft · unverified_draft

   ### bg-oral-glucan-does-reach-the-blood Maximum plasma concentrations for glucan phosphate occurred at 4 hours while laminarin and scleroglucan showed two plasma peaks between 0.5 and 12 hours, at 24 hours 27 plus or minus 3% of the glucan phosphate and 20 plus or minus 7% of the laminarin remained in the serum, following oral administration glucans were bound and internalized by intestinal epithelial cells and gut-associated lymphoid tissue cells with internalization by intestinal epithelial cells not being Dectin-dependent, gut-associated lymphoid tissue expression of Dectin-1 and Toll-like receptor 2 but not Toll-like receptor 4 increased, oral glucan increased systemic levels of interleukin-12 by 151%, and oral glucan administration also increased survival in mice challenged with Staphylococcus aureus or Candida albicans. 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: In rodents the swallowed sugar does cross into the circulation, is taken up by the gut immune tissue, and leaves the animals better able to survive an infection. organism: Rat and mouse tissue_or_cell_type: Plasma, intestinal epithelium and gut-associated lymphoid tissue experimental_model: Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice limitations: Rodent pharmacokinetics and rodent challenge models. The reported figure for glucan phosphate at 24 hours is a percentage remaining in serum whose denominator the abstract does not state, so it is not read here as a fraction of the swallowed dose. exposure: Glucan phosphate, laminarin and scleroglucan at 1 milligram per kilogram orally in rats, and 1 milligram orally in mice evidence_span: {"source_cache": "artifacts/glucan-research/15976018.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18", "start_char": 0, "end_char": 1617, "text_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18"} [bg-p15976018] Oral delivery and gastrointestinal absorption of soluble glucans stimulate increased resistance to infectious challenge. (2005). https://pubmed.ncbi.nlm.nih.gov/15976018/ DOI: 10.1124/jpet.105.085415

   Complete structured claim and evidence

3. Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms.

   Beta-glucan → Trained immunity, an altered response to a later challenge after the first has ended source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"}

   experimental_model

   Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo

   exposure

   Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge

   limitations

   The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route.

   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

   Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired.

   primary_references

   [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006

   tissue_or_cell_type

   Monocyte

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 424–435

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo · source_derived_draft · unverified_draft

   ### bg-training-runs-through-raf1 Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms. 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: Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired. organism: Mouse tissue_or_cell_type: Monocyte experimental_model: Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo limitations: The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route. exposure: Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge evidence_span: {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"} [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006

   Complete structured claim and evidence