ArticleInfection and immunity1994
Candida albicans stimulates arachidonic acid liberation from alveolar macrophages through alpha-mannan and beta-glucan cell wall components.
Article in Infection and immunity, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 71 citations in OpenAlex.
- Host albumin redirects Candida albicans metabolism to engage an alternative pathogenicity pathway.Nature communications · 2025Article
- Review
- Bioactive lipid-based therapeutic approach to COVID-19 and other similar infections.Archives of medical science : AMS · 2023Article
- Complex and Controversial Roles of Eicosanoids in Fungal Pathogenesis.Journal of fungi (Basel, Switzerland) · 2021Review
- Effect of dietary β-1,3-glucan supplementation and heat stress on growth performance, nutrient digestibility, meat quality, organ weight, ileum microbiota, and immunity in broilers.Poultry science · 2020Article
- Fungal Symbionts Produce Prostaglandin EFrontiers in cellular and infection microbiology · 2019Article
- Prostaglandin EPharmacology & therapeutics · 2018Review
- Dectin-2 Is a C-Type Lectin Receptor that Recognizes Pneumocystis and Participates in Innate Immune Responses.American journal of respiratory cell and molecular biology · 2018Article
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- Candida albicans and Pseudomonas aeruginosa Interaction, with Focus on the Role of Eicosanoids.Frontiers in physiology · 2016Review
- Leukotrienes target F-actin/cofilin-1 to enhance alveolar macrophage anti-fungal activity.The Journal of biological chemistry · 2011Article
- Characterization of prostaglandin E2 production by Candida albicans.Infection and immunity · 2007Article
- Cytotoxic and cytokine-inducing properties of Candida glabrata in single and mixed oral infection models.Microbial pathogenesis · 2007Article
- Cryptococcal phospholipases: a novel lysophospholipase discovered in the pathogenic fungus Cryptococcus gattii.The Biochemical journal · 2004Article
- Transcriptional response of Candida albicans upon internalization by macrophages.Eukaryotic cell · 2004Article
- Surface glycans of Candida albicans and other pathogenic fungi: physiological roles, clinical uses, and experimental challenges.Clinical microbiology reviews · 2004Review
- Production of eicosanoids and other oxylipins by pathogenic eukaryotic microbes.Clinical microbiology reviews · 2003Review
- Immunology of diseases associated with Malassezia species.Clinical microbiology reviews · 2002Review
- beta-1,2-linked oligomannosides from Candida albicans bind to a 32-kilodalton macrophage membrane protein homologous to the mammalian lectin galectin-3.Infection and immunity · 2000Article
- Candida albicans-derived beta-1,2-linked mannooligosaccharides induce desensitization of macrophages.Infection and immunity · 2000Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Candida albicans is an increasingly important fungal pathogen. Alveolar macrophages respond to fungal components such as zymosan by releasing arachidonic acid (AA) and AA metabolites. However, few studies hypothesized that macrophages respond to C. albicans by releasing AA and generating AA metabolites as a consequence of interaction of mannose and beta-glucan receptors with fungal cell wall components. [14C]AA-labeled rabbit alveolar macrophages released AA following stimulation with either live or heat-killed C. albicans. High-pressure liquid chromatography analysis revealed that 55% of the AA released was metabolized via cyclooxygenase and lipoxygenase pathways. The metabolites consisted of prostaglandin E2, prostaglandin F2 alpha, 6-ketoprostaglandin F1 alpha, thromboxane B2, and leukotrienes B4 and D4. We further examined the roles of alpha-mannan and beta-glucan components of C. albicans in mediating these alterations of eicosanoid metabolism. Prior work in our laboratory has shown that soluble alpha-mannan and beta-glucan inhibit macrophage mannose and beta-glucan receptors, respectively. Incubation of alveolar macrophages with soluble alpha-mannan derived from C. albicans (1 mg/ml) resulted in 49.8% +/- 2.6% inhibition of macrophage AA release during stimulation with intact C. albicans (P = 0.0001 versus control). Macrophage AA release in response to C. albicans was also inhibited to a significant but lesser degree by soluble beta-glucan (36.2% +/- 1.3%; P = 0.008 versus control). These results indicate that C. albicans stimulates macrophage AA metabolism and that these effects are partly mediated by alpha-mannan and beta-glucan constituents of the fungus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.