ArticleInfection and immunity2004
Fungal metabolite gliotoxin inhibits assembly of the human respiratory burst NADPH oxidase.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
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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
60 citing papers in PubMed, 139 citations in OpenAlex.
- Gliotoxin Production and Self-Defense in Filamentous Fungi.Annual review of microbiology · 2025Review
- Progress in Gliotoxin Research.Molecules (Basel, Switzerland) · 2025Review
- Natural compounds-based nanomedicines for cancer treatment: Future directions and challenges.Drug delivery and translational research · 2024Review
- Aspergillus fumigatus mitogen-activated protein kinase MpkA is involved in gliotoxin production and self-protection.Nature communications · 2024Article
- Article
- Epipolythiodioxopiperazine-Based Natural Products: Building Blocks, Biosynthesis and Biological Activities.Chembiochem : a European journal of chemical biology · 2022Review
- Regulation of gliotoxin biosynthesis and protection in Aspergillus species.PLoS genetics · 2022Article
- The Toxic Mechanism of Gliotoxins and Biosynthetic Strategies for Toxicity Prevention.International journal of molecular sciences · 2021Review
- Article
- Review
- Fungal immunity and pathogenesis in mammals versus the invertebrate model organism Galleria mellonella.Pathogens and disease · 2021Review
- The Pathogenesis ofPolish journal of microbiology · 2021Review
- Fungal Toxins and Host Immune Responses.Frontiers in microbiology · 2021Review
- Sensing the threat posed by Aspergillus infection.Current opinion in microbiology · 2020Review
- The Aspergillus fumigatus transcription factor RglT is important for gliotoxin biosynthesis and self-protection, and virulence.PLoS pathogens · 2020Article
- Mycoparasitism illuminated by genome and transcriptome sequencing ofMicrobial genomics · 2020Article
- The role of NOX inhibitors in neurodegenerative diseases.IBRO reports · 2019Review
- Intracellular Delivery of Biologically-Active Fungal Metabolite Gliotoxin Using Magnetic Nanoparticles.Materials (Basel, Switzerland) · 2019Article
- Redox Activation of Nox1 (NADPH Oxidase 1) Involves an Intermolecular Disulfide Bond Between Protein Disulfide Isomerase and p47Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Characterization ofFrontiers in microbiology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species are a critical weapon in the killing of Aspergillus fumigatus by polymorphonuclear leukocytes (PMN), as demonstrated by severe aspergillosis in chronic granulomatous disease. In the present study, A. fumigatus-produced mycotoxins (fumagillin, gliotoxin [GT], and helvolic acid) are examined for their effects on the NADPH oxidase activity in human PMN. Of these mycotoxins, only GT significantly and stoichiometrically inhibits phorbol myristate acetate (PMA)-stimulated O2- generation, while the other two toxins are ineffective. The inhibition is dependent on the disulfide bridge of GT, which interferes with oxidase activation but not catalysis of the activated oxidase. Specifically, GT inhibits PMA-stimulated events: p47phox phosphorylation, its incorporation into the cytoskeleton, and the membrane translocation of p67phox, p47phox, and p40phox, which are crucial steps in the assembly of the active NADPH oxidase. Thus, damage to p47phox phosphorylation is likely a key to inhibiting NADPH oxidase activation. GT does not inhibit the membrane translocation of Rac2. The inhibition of p47phox phosphorylation is due to the defective membrane translocation of protein kinase C (PKC) betaII rather than an effect of GT on PKC betaII activity, suggesting a failure of PKC betaII to associate with the substrate, p47phox, on the membrane. These results suggest that A. fumigatus may confront PMN by inhibiting the assembly of the NADPH oxidase with its hyphal product, GT.
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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.