ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Cryptococcus neoformans-induced macrophage lysosome damage crucially contributes to fungal virulence.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed.
- Set202 is a histone lysine methyltransferase that enablesbioRxiv : the preprint server for biology · 2026Article
- Glycoprotein-induced phase separation drives unconventional secretion of galectin-3.Nature communications · 2026Article
- Organ-specific immune responses are strain-dependent in a mouse model ofMicrobiology spectrum · 2026Article
- Use of a human immortalized microglia cell line to study recognition, phagocytosis, and intracellular survival ofmSphere · 2026Article
- Article
- Degradation of oxidized phospholipids by lysosomal phospholipase A2 regulates pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Insights from Mass Spectrometry-Based Proteomics onJournal of fungi (Basel, Switzerland) · 2025Review
- Elements of dissemination in cryptococcosis.mBio · 2024Review
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- Host-Pathogen Interactions and Correlated Factors That Are Affected in Replicative-AgedJournal of fungi (Basel, Switzerland) · 2024Article
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
- Kicking sleepers out of bed: Macrophages promote reactivation of dormant Cryptococcus neoformans by extracellular vesicle release and non-lytic exocytosis.PLoS pathogens · 2023Article
- Fungal mechanisms of intracellular survival: what can we learn from bacterial pathogens?Infection and immunity · 2023Review
- Innate Pulmonary Phagocytes and Their Interactions with PathogenicJournal of fungi (Basel, Switzerland) · 2023Review
- "Under Pressure" - How fungi evade, exploit, and modulate cells of the innate immune system.Seminars in immunology · 2023Review
- Streptococcus agalactiaemBio · 2022Article
- Streptococcus agalactiae cadD alleviates metal stress and promotes intracellular survival in macrophages and ascending infection during pregnancy.Nature communications · 2022Article
- Protective interaction of human phagocytic APC subsets withFrontiers in immunology · 2022Article
- Real-time visualization of phagosomal pH manipulation byFrontiers in cellular and infection microbiology · 2022Article
- A new humanized antibody is effective against pathogenic fungi in vitro.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Upon ingestion by macrophages, Cryptococcus neoformans can survive and replicate intracellularly unless the macrophages become classically activated. The mechanism enabling intracellular replication is not fully understood; neither are the mechanisms that allow classical activation to counteract replication. C. neoformans-induced lysosome damage was observed in infected murine bone marrow-derived macrophages, increased with time, and required yeast viability. To demonstrate lysosome damage in the infected host, we developed a novel flow cytometric method for measuring lysosome damage. Increased lysosome damage was found in C. neoformans-containing lung cells compared with C. neoformans-free cells. Among C. neoformans-containing myeloid cells, recently recruited cells displayed lower damage than resident cells, consistent with the protective role of recruited macrophages. The magnitude of lysosome damage correlated with increased C. neoformans replication. Experimental induction of lysosome damage increased C. neoformans replication. Activation of macrophages with IFN-γ abolished macrophage lysosome damage and enabled increased killing of C. neoformans. We conclude that induction of lysosome damage is an important C. neoformans survival strategy and that classical activation of host macrophages counters replication by preventing damage. Thus, therapeutic strategies that decrease lysosomal damage, or increase resistance to such damage, could be valuable in treating cryptococcal infections.
Indexed as
Identifiers
What OpenQuestion holds
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.