ArticleThe Journal of infectious diseases2016
β-Glucans Are Masked but Contribute to Pulmonary Inflammation During Pneumocystis Pneumonia.
Article in The Journal of infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- A diagnostic model for discrimination between Pneumocystis jirovecii pneumonia and colonization based on multiple parameters.Scientific reports · 2026Article
- Strain-Dependent Protective Innate Immunity AgainstJournal of fungi (Basel, Switzerland) · 2026Article
- The importance of Fcγ and C-type lectin receptors in host immune responses duringInfection and immunity · 2025Article
- CD40 Expression by B Cells Is Required for Optimal Immunity to Murine Pneumocystis Infection.The Journal of infectious diseases · 2024Article
- Preclinical and Toxicology Assessment of ALW-II-41-27, an Inhibitor of the Eph Receptor A2 (EphA2).Drugs in R&D · 2024Article
- Retracing the evolution ofMicrobiology and molecular biology reviews : MMBR · 2024Review
- High prevalence of pneumocystis pneumonia in interstitial lung disease: a retrospective study.Infection · 2024Article
- Targeting host tyrosine kinase receptor EphA2 signaling via small-molecule ALW-II-41-27 inhibits macrophage pro-inflammatory signaling responses toAntimicrobial agents and chemotherapy · 2024Article
- CD40 Expression by B cells is Required for Optimal Immunity to MurinebioRxiv : the preprint server for biology · 2024Article
- Meta-Analysis and Systematic Literature Review of the GenusJournal of fungi (Basel, Switzerland) · 2023Article
- Axenic Long-Term Cultivation ofJournal of fungi (Basel, Switzerland) · 2023Article
- Targeting β-glucans, vital components of theFrontiers in immunology · 2023Review
- Article
- EphA2 Is a Lung Epithelial Cell Receptor for Pneumocystis β-Glucans.The Journal of infectious diseases · 2022Article
- A Novel Encochleated Formulation Improves Atovaquone Activity in a Murine Model of Pneumocystis Pneumonia.The Journal of infectious diseases · 2021Article
- Survey of the Transcription Factor Responses of Mouse Lung Alveolar Macrophages toPathogens (Basel, Switzerland) · 2021Article
- Targeting CARD9 with Small-Molecule Therapeutics Inhibits Innate Immune Signaling and Inflammatory Response to Pneumocystis carinii β-Glucans.Antimicrobial agents and chemotherapy · 2020Article
- Pneumocystis carinii Major Surface Glycoprotein Dampens Macrophage Inflammatory Responses to Fungal β-Glucan.The Journal of infectious diseases · 2020Article
- MUC1 mediates Pneumocystis murina binding to airway epithelial cells.Cellular microbiology · 2020Article
- Evaluation of a PCR-electrospray ionization mass spectrometry platform for detection and identification of fungal pathogens directly from prospectively collected bronchoalveolar lavage specimens.Diagnostic microbiology and infectious disease · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
β-glucans, which can activate innate immune responses, are a major component in the cell wall of the cyst form of Pneumocystis In the current study, we examined whether β-1,3-glucans are masked by surface proteins in Pneumocystis and what role β-glucans play in Pneumocystis-associated inflammation. For 3 species, including Pneumocystis jirovecii, which causes Pneumocystis pneumonia in humans, Pneumocystis carinii, and Pneumocystis murina, β-1,3-glucans were masked in most organisms, as demonstrated by increased exposure following trypsin treatment. Using quantitative polymerase chain reaction and microarray techniques, we demonstrated in a mouse model of Pneumocystis pneumonia that treatment with caspofungin, an inhibitor of β-1,3-glucan synthesis, for 21 days decreased expression of a broad panel of inflammatory markers, including interferon γ, tumor necrosis factor α, interleukin 1β, interleukin 6, and multiple chemokines/chemokine ligands. Thus, β-glucans in Pneumocystis cysts are largely masked, which likely decreases innate immune activation; this mechanism presumably was developed for interactions with immunocompetent hosts, in whom organism loads are substantially lower. In immunosuppressed hosts with a high organism burden, organism death and release of glucans appears to be an important contributor to deleterious host inflammatory responses.
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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.