ArticleInfection and immunity2015
The Granuloma Response Controlling Cryptococcosis in Mice Depends on the Sphingosine Kinase 1-Sphingosine 1-Phosphate Pathway.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 29 citations in OpenAlex.
- Subunits of adaptor protein complex-1 make distinct contributions to the virulence ofInfection and immunity · 2026Article
- Immunological mechanism behind reactivated cryptococcosis in persistently infected mice following FTY720 treatment.Infection and immunity · 2026Article
- Alternatively activated monocyte-derived myeloid cells promote extracellular pathogen persistence in pulmonary fungal granulomas.The Journal of experimental medicine · 2026Article
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- Signaling controversy and future therapeutical perspectives of targeting sphingolipid network in cancer immune editing and resistance to tumor necrosis factor-α immunotherapy.Cell communication and signaling : CCS · 2024Review
- Role of sphingolipids in the host-pathogen interaction.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023Article
- Kicking sleepers out of bed: Macrophages promote reactivation of dormant Cryptococcus neoformans by extracellular vesicle release and non-lytic exocytosis.PLoS pathogens · 2023Article
- An Immunogenic and Slow-Growing Cryptococcal Strain Induces a Chronic Granulomatous Infection in Murine Lungs.Infection and immunity · 2022Article
- The granuloma in cryptococcal disease.PLoS pathogens · 2021Review
- Bioactive sphingolipids: Advancements and contributions from the laboratory of Dr. Lina M. Obeid.Cellular signalling · 2021Review
- FTY720 reactivates cryptococcal granulomas in mice through S1P receptor 3 on macrophages.The Journal of clinical investigation · 2020Article
- Article
- Animal Models ofFrontiers in immunology · 2020Review
- Sphingosine-1-phosphate receptors and innate immunity.Cellular microbiology · 2018Review
- Mechanisms of Pulmonary Escape and Dissemination by Cryptococcus neoformans.Journal of fungi (Basel, Switzerland) · 2018Review
- An insight into new strategies to combat antifungal drug resistance.Drug design, development and therapy · 2018Review
- Analysis of sphingolipids, sterols, and phospholipids in human pathogenicJournal of lipid research · 2017Article
- Sphingolipids in neutrophil function and inflammatory responses: Mechanisms and implications for intestinal immunity and inflammation in ulcerative colitis.Advances in biological regulation · 2017Review
- Sphingolipids as targets for treatment of fungal infections.Future medicinal chemistry · 2016Review
- Activation-Induced Cell Death of Dendritic Cells Is Dependent on Sphingosine Kinase 1.Frontiers in pharmacology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cryptococcus neoformans is a fungal pathogen that causes pulmonary infections, which may progress into life-threatening meningitis. In commonly used mouse models of C. neoformans infections, fungal cells are not contained in the lungs, resulting in dissemination to the brain. We have previously reported the generation of an engineered C. neoformans strain (C. neoformans Δgcs1) which can be contained in lung granulomas in the mouse model and have shown that granuloma formation is dependent upon the enzyme sphingosine kinase 1 (SK1) and its product, sphingosine 1-phosphate (S1P). In this study, we have used four mouse models, CBA/J and C57BL6/J (both immunocompetent), Tgε26 (an isogenic strain of strain CBA/J lacking T and NK cells), and SK(-/-) (an isogenic strain of strain C57BL6/J lacking SK1), to investigate how the granulomatous response and SK1-S1P pathway are interrelated during C. neoformans infections. S1P and monocyte chemotactic protein-1 (MCP-1) levels were significantly elevated in the bronchoalveolar lavage fluid of all mice infected with C. neoformans Δgcs1 but not in mice infected with the C. neoformans wild type. SK1(-/-) mice did not show elevated levels of S1P or MCP-1. Primary neutrophils isolated from SK1(-/-) mice showed impaired antifungal activity that could be restored by the addition of extracellular S1P. In addition, high levels of tumor necrosis factor alpha were found in the mice infected with C. neoformans Δgcs1 in comparison to the levels found in mice infected with the C. neoformans wild type, and their levels were also dependent on the SK1-S1P pathway. Taken together, these results suggest that the SK1-S1P pathway promotes host defense against C. neoformans infections by regulating cytokine levels, promoting extracellular killing by phagocytes, and generating a granulomatous response.
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