ArticlePLoS pathogens2019
15-keto-prostaglandin E2 activates host peroxisome proliferator-activated receptor gamma (PPAR-γ) to promote Cryptococcus neoformans growth during infection.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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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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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Gut microbiota in chronic inflammation: the interplay with lipid mediators.Gut microbes · 2026Review
- Candida albicans Cells Lacking AP-2 Have Defective Hyphae and Are Avirulent Despite Increased Host Uptake and Intracellular Proliferation in Macrophages.Molecular microbiology · 2026Article
- Exploring Oxylipins in Host-Microbe Interactions and Their Impact on Infection and Immunity.Current issues in molecular biology · 2025Review
- Immunometabolic reprogramming in macrophages infected with active and dormantInfection and immunity · 2025Article
- Selenium, Immunity, and Inflammatory Bowel Disease.Nutrients · 2024Review
- Preclinical Models for Cryptococcosis of the CNS and Their Characterization Using In Vivo Imaging Techniques.Journal of fungi (Basel, Switzerland) · 2024Review
- Models for Inducing Experimental Cryptococcosis in Mice.Methods in molecular biology (Clifton, N.J.) · 2024Article
- TRAIL promotes the polarization of human macrophages toward a proinflammatory M1 phenotype and is associated with increased survival in cancer patients with high tumor macrophage content.Frontiers in immunology · 2023Article
- Zebrafish Larvae as an Experimental Model of Cryptococcal Meningitis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation.Developmental cell · 2022Article
- Blood vessel occlusion by Cryptococcus neoformans is a mechanism for haemorrhagic dissemination of infection.PLoS pathogens · 2022Article
- Cyclooxygenase production of PGE2 promotes phagocyte control of A. fumigatus hyphal growth in larval zebrafish.PLoS pathogens · 2022Article
- Mapping Mechanistic Pathways of Acute Oral Systemic Toxicity Using Chemical Structure and Bioactivity Measurements.Frontiers in toxicology · 2022Article
- Gestational long-term hypoxia induces metabolomic reprogramming and phenotypic transformations in fetal sheep pulmonary arteries.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Complex and Controversial Roles of Eicosanoids in Fungal Pathogenesis.Journal of fungi (Basel, Switzerland) · 2021Review
- Article
- Correction: 15-keto-prostaglandin E2 activates host peroxisome proliferator-activated receptor gamma (PPAR-γ) to promote Cryptococcus neoformans growth during infection.PLoS pathogens · 2020Article
- Solid-state NMR spectroscopy identifies three classes of lipids inThe Journal of biological chemistry · 2020Article
- PPAR-gamma Fun(gi) With Prostaglandin.Nuclear receptor signaling · 2020Article
- Article
Corrections and comments
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- Erratum issued
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Cryptococcus neoformans is one of the leading causes of invasive fungal infection in humans worldwide. C. neoformans uses macrophages as a proliferative niche to increase infective burden and avoid immune surveillance. However, the specific mechanisms by which C. neoformans manipulates host immunity to promote its growth during infection remain ill-defined. Here we demonstrate that eicosanoid lipid mediators manipulated and/or produced by C. neoformans play a key role in regulating pathogenesis. C. neoformans is known to secrete several eicosanoids that are highly similar to those found in vertebrate hosts. Using eicosanoid deficient cryptococcal mutants Δplb1 and Δlac1, we demonstrate that prostaglandin E2 is required by C. neoformans for proliferation within macrophages and in vivo during infection. Genetic and pharmacological disruption of host PGE2 synthesis is not required for promotion of cryptococcal growth by eicosanoid production. We find that PGE2 must be dehydrogenated into 15-keto-PGE2 to promote fungal growth, a finding that implicated the host nuclear receptor PPAR-γ. C. neoformans infection of macrophages activates host PPAR-γ and its inhibition is sufficient to abrogate the effect of 15-keto-PGE2 in promoting fungal growth during infection. Thus, we describe the first mechanism of reliance on pathogen-derived eicosanoids in fungal pathogenesis and the specific role of 15-keto-PGE2 and host PPAR-γ in cryptococcosis.
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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.