ArticleMicrobiology (Reading, England)2012
Blood-brain barrier invasion by Cryptococcus neoformans is enhanced by functional interactions with plasmin.
Article in Microbiology (Reading, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 53 citations in OpenAlex.
- Pathogenicity and virulence of the blast fungusVirulence · 2026Review
- Nanotechnology-powered Meningitis Therapies: Lipid Nanoparticles Lead the Way.Current pharmaceutical biotechnology · 2025Review
- Clinical characteristics and prognostic factors of pulmonary and extrapulmonary cryptococcosis.BMC infectious diseases · 2024Article
- Mechanisms and Virulence Factors ofJournal of fungi (Basel, Switzerland) · 2024Review
- The pathways and the mechanisms by whichMycology · 2024Review
- Review
- Mechanisms of fungal dissemination.Cellular and molecular life sciences : CMLS · 2021Review
- Fibrinolysis: A Primordial System Linked to the Immune Response.International journal of molecular sciences · 2021Review
- PreventingEmerging microbes & infections · 2020Article
- A critical role for plasminogen in inflammation.The Journal of experimental medicine · 2020Review
- Toxoflavin Produced byApplied and environmental microbiology · 2019Article
- Plasminogen-binding proteins as an evasion mechanism of the host's innate immunity in infectious diseases.Bioscience reports · 2018Review
- Pathogen interactions with endothelial cells and the induction of innate and adaptive immunity.European journal of immunology · 2018Review
- The plasminogen binding protein PbsP is required for brain invasion by hypervirulent CC17 Group B streptococci.Scientific reports · 2018Article
- Innate immune evasion strategies against Cryptococcal meningitis caused byExperimental and therapeutic medicine · 2017Article
- Complex Roles of Annexin A2 in Host Blood-Brain Barrier Invasion by Cryptococcus neoformans.CNS neuroscience & therapeutics · 2017Article
- Pulmonary Cryptococcosis in the Immunocompetent Patient-Many Questions, Some Answers.Open forum infectious diseases · 2016Article
- Systemic Approach to Virulence Gene Network Analysis for Gaining New Insight into Cryptococcal Virulence.Frontiers in microbiology · 2016Article
- Diagnostic Challenges of Cryptococcus neoformans in an Immunocompetent Individual Masquerading as Chronic Hydrocephalus.Case reports in neurological medicine · 2016Article
- Dissociation of Tissue Destruction and Bacterial Expansion during Bubonic Plague.PLoS pathogens · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cryptococcus neoformans can invade the central nervous system through diverse mechanisms. We examined a possible role for host plasma proteases in the neurotropic behaviour of this blood-borne fungal pathogen. Plasminogen is a plasma-enriched zymogen that can passively coat the surface of blood-borne pathogens and, upon conversion to the serine protease plasmin, facilitate pathogen dissemination by degrading vascular barriers. In this study, plasminogen-to-plasmin conversion on killed and viable hypoencapsulated strains of C. neoformans required the addition of plasminogen activator (PA), but this conversion occurred in the absence of supplemented PA when viable strains were cultured with brain microvascular endothelial cells (BMEC). Plasmin-coated C. neoformans showed an enhanced invasive ability in Matrigel invasion assays that was significantly augmented in the presence of BMEC. The invasive effect of plasmin required viable pathogen and correlated with rapid declines in BMEC barrier function. Plasmin-enhanced invasion was inhibited by aprotinin, carboxypeptidase B, the lysine analogue epsilon-aminocaproic acid, and by capsule development. C. neoformans caused plasminogen-independent declines in BMEC barrier function that were associated with pathogen-induced host damage; however, such declines were significantly delayed and less extensive than those observed with plasmin-coated pathogen. BMEC adhesion and damage by hypoencapsulated C. neoformans were diminished by capsule induction but unaltered by plasminogen and/or PA. We conclude that hypoencapsulated C. neoformans can invade BMEC by a plasmin-dependent mechanism, in vitro, and that small, or minimal, surface capsule expression during the blood-borne phase of cryptococcosis may promote virulence by means of plasmin(ogen) acquisition.
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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.