ArticleInfection and immunity2016
Real-Time Imaging of Interactions of Neutrophils with Cryptococcus neoformans Demonstrates a Crucial Role of Complement C5a-C5aR Signaling.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
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
26 citing papers in PubMed, 41 citations in OpenAlex.
- Blood neutrophil counts in HIV-infected patients with cryptococcal meningitis: Association with mortality.PloS one · 2018Trial
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Reactive oxygen species drive the aberrant immune response to aFrontiers in immunology · 2025Article
- CD146 deficiency promotes inflammatory type 2 responses in pulmonary cryptococcosis.Medical microbiology and immunology · 2023Article
- Innate Pulmonary Phagocytes and Their Interactions with PathogenicJournal of fungi (Basel, Switzerland) · 2023Review
- A comparative study of IL-33 and its receptor ST2 in a C57BL/6 J mouse model of pulmonary Cryptococcus neoformans infection.Medical microbiology and immunology · 2023Article
- Article
- Genome-scale CRISPR screening reveals that C3aR signaling is critical for rapid capture of fungi by macrophages.PLoS pathogens · 2022Article
- Allicin shows antifungal efficacy againstFrontiers in microbiology · 2022Article
- Review
- Clinical Diagnosis, Treatment, and Laboratory Detection of 50 Cases of Pulmonary Cryptococcosis.Computational and mathematical methods in medicine · 2022Article
- Central Nervous System Cryptococcosis in Patients With Sarcoidosis: Comparison With Non-sarcoidosis Patients and Review of Potential Pathophysiological Mechanisms.Frontiers in medicine · 2022Article
- Mechanisms of fungal dissemination.Cellular and molecular life sciences : CMLS · 2021Review
- Mechanisms of PathogenicFrontiers in cellular and infection microbiology · 2020Review
- Fungal dissemination is limited by liver macrophage filtration of the blood.Nature communications · 2019Article
- Nonlytic exocytosis of Cryptococcus neoformans from neutrophils in the brain vasculature.Cell communication and signaling : CCS · 2019Article
- Innate Immunity against Cryptococcus, from Recognition to Elimination.Journal of fungi (Basel, Switzerland) · 2018Review
- Host response to pulmonary fungal infections: A highlight on cell-driven immunity toCurrent pharmacology reports · 2017Article
- Innate Immune Responses toJournal of fungi (Basel, Switzerland) · 2017Article
- Increased activity of the complement system in cerebrospinal fluid of the patients with Non-HIV Cryptococcal meningitis.BMC infectious diseases · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Neutrophils have been shown to efficiently kill Cryptococcus neoformans, a causative agent of meningoencephalitis. Here, using live-cell imaging, we characterize the dynamic interactions of neutrophils with C. neoformans and the underlying mechanisms in real time. Neutrophils were directly seen to chase C. neoformans cells and then rapidly internalize them. Complement C5a-C5aR signaling guided neutrophils to migrate to the yeast cells, resulting in optimal phagocytosis and subsequent killing of the organisms. The addition of recombinant complement C5a enhanced neutrophil movement but did not induce chemotaxis, suggesting that the C5a gradient is crucial. Incubation with C. neoformans resulted in enhanced activation of Erk and p38 mitogen-activated protein (MAP) kinases (MAPKs) in neutrophils. Inhibition of the p38 MAPK pathway, but not the Erk pathway, significantly impaired neutrophil migration and its subsequent killing of C. neoformans. Deficiency of CD11b or blocking of CD11b did not affect the migration of neutrophils toward C. neoformans but almost completely abolished phagocytosis and killing of the organisms by neutrophils. C5a-C5aR signaling induced enhanced surface expression of CD11b. Interestingly, the original surface expression of CD11b was essential and sufficient for neutrophils to attach to C. neoformans but was unable to mediate phagocytosis. In contrast, the enhanced surface expression of CD11b induced by C5a-C5aR signaling was essential for neutrophil phagocytosis and subsequent killing of yeast cells. Collectively, this is the first report of the dynamic interactions of neutrophils with C. neoformans, demonstrating a crucial role of C5a-C5aR signaling in neutrophil killing of C. neoformans in real time.
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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.