ArticleCommunications biology2021
Cell wall N-glycan of Candida albicans ameliorates early hyper- and late hypo-immunoreactivity in sepsis.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Rethinking the immune recognition of cell walls in human fungal pathogens: Mechanisms, controversies and translational significance.Virulence · 2026Review
- Untargeted Metabolomic Analysis of Cell-Free Supernatants (CFSs) from Different Clinical Isolates ofJournal of fungi (Basel, Switzerland) · 2026Article
- Cas5 Regulates the Exposure of β-Glucan, the Cell Surface Hydrophobicity, and the Expression of Cell Wall Proteins to Remodel theMicroorganisms · 2025Article
- Impact of different pathogen classes on the serumBBA advances · 2025Article
- An immune-adrenergic pathway induces lethal levels of platelet-activating factor in mice.Communications biology · 2024Article
- The FVirulence · 2023Article
- Pathogenesis and virulence ofVirulence · 2022Review
- Immunological hyporesponsiveness in tuberculosis: The role of mycobacterial glycolipids.Frontiers in immunology · 2022Review
- Defective antifungal immunity in patients with COVID-19.Frontiers in immunology · 2022Review
- Translational and Clinical Significance of DAMPs, PAMPs, and PRRs in Trauma-induced Inflammation.Archives of clinical and biomedical research · 2022Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe infection often causes a septic cytokine storm followed by immune exhaustion/paralysis. Not surprisingly, many pathogens are equipped with various anti-inflammatory mechanisms. Such mechanisms might be leveraged clinically to control septic cytokine storms. Here we show that N-glycan from pathogenic C. albicans ameliorates mouse sepsis through immunosuppressive cytokine IL-10. In a sepsis model using lipopolysaccharide (LPS), injection of the N-glycan upregulated serum IL-10, and suppressed pro-inflammatory IL-1β, TNF-α and IFN-γ. The N-glycan also improved the survival of mice challenged by LPS. Analyses of structurally defined N-glycans from several yeast strains revealed that the mannose core is key to the upregulation of IL-10. Knocking out the C-type lectin Dectin-2 abrogated the N-glycan-mediated IL-10 augmentation. Furthermore, C. albicans N-glycan ameliorated immune exhaustion/immune paralysis after acute inflammation. Our results suggest a strategy where the immunosuppressive mechanism of one pathogen can be applied to attenuate a severe inflammation/cytokine storm caused by another pathogen.
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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.