ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.
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. An erratum has been issued. Cited by 39 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
39 citing papers in PubMed, 53 citations in OpenAlex.
- Immune Modulation and Evasion byACS omega · 2026Review
- Advances in cryptococcal infections-associated immunopathology and potential therapeutic strategies.Frontiers in pharmacology · 2026Review
- Apoptosis as an evolutionary battleground: pathogen pressure and the shaping of programmed cell death pathways.Frontiers in cell and developmental biology · 2026Review
- Histone demethylase LSD1 regulates lipid homeostasis duringiScience · 2025Article
- Immunometabolic reprogramming in macrophages infected with active and dormantInfection and immunity · 2025Article
- Pathogen-induced mitochondrial dysfunction: mechanistic insights, immune crosstalk, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Assessing Phagocytosis of Cryptococcus neoformans Cells in Human Monocytes or the J774 Murine Macrophage Cell Line.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Macrophage variants in laboratory research: most are well done, but some are RAW.Frontiers in cellular and infection microbiology · 2024Review
- CD146 deficiency promotes inflammatory type 2 responses in pulmonary cryptococcosis.Medical microbiology and immunology · 2023Article
- "Under Pressure" - How fungi evade, exploit, and modulate cells of the innate immune system.Seminars in immunology · 2023Review
- Calcimycin InhibitsACS infectious diseases · 2022Article
- Review
- Article
- Cholesterol and sphingomyelin are critical for Fcγ receptor-mediated phagocytosis of Cryptococcus neoformans by macrophages.The Journal of biological chemistry · 2021Article
- Cryptococcus neoformansmBio · 2021Article
- Transcriptomic analysis reveals that mTOR pathway can be modulated in macrophage cells by the presence of cryptococcal cells.Genetics and molecular biology · 2021Article
- From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways.Computational and structural biotechnology journal · 2021Review
- Monitoring Glycolysis and Respiration Highlights Metabolic Inflexibility ofPathogens (Basel, Switzerland) · 2020Article
- Macrophages use a bet-hedging strategy for antimicrobial activity in phagolysosomal acidification.The Journal of clinical investigation · 2020Article
- CoremBio · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 5 countries.
Funding
Abstract
Human infection with Cryptococcus neoformans, a common fungal pathogen, follows deposition of yeast spores in the lung alveoli. The subsequent host-pathogen interaction can result in eradication, latency, or extrapulmonary dissemination. Successful control of C. neoformans infection is dependent on host macrophages, but macrophages display little ability to kill C. neoformans in vitro. Recently, we reported that ingestion of C. neoformans by mouse macrophages induces early cell cycle progression followed by mitotic arrest, an event that almost certainly reflects host cell damage. The goal of the present work was to understand macrophage pathways affected by C. neoformans toxicity. Infection of macrophages by C. neoformans was associated with alterations in protein translation rate and activation of several stress pathways, such as hypoxia-inducing factor-1-α, receptor-interacting protein 1, and apoptosis-inducing factor. Concomitantly we observed mitochondrial depolarization in infected macrophages, an observation that was replicated in vivo. We also observed differences in the stress pathways activated, depending on macrophage cell type, consistent with the nonspecific nature of C. neoformans virulence known to infect phylogenetically distant hosts. Our results indicate that C. neoformans infection impairs multiple host cellular functions and undermines the health of these critical phagocytic cells, which can potentially interfere with their ability to clear this fungal pathogen.
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.