ArticlePLoS pathogens2022
Bet-hedging antimicrobial strategies in macrophage phagosome acidification drive the dynamics of Cryptococcus neoformans intracellular escape mechanisms.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Immune Modulation and Evasion byACS omega · 2026Review
- Review
- A conserved enzymatic toolkit targeting host cell metabolism is associated with Cryptococcus neoformans intracellular survival in protozoal and mammalian phagocytic cells.PLoS pathogens · 2025Article
- A method for authenticating the fidelity ofMicrobiology spectrum · 2025Article
- Article
- Host-Pathogen Interactions and Correlated Factors That Are Affected in Replicative-AgedJournal of fungi (Basel, Switzerland) · 2024Article
- A food color based colorimetric assay forbioRxiv : the preprint server for biology · 2024Article
- Survival in macrophages induces enhanced virulence inmSphere · 2024Article
- 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
- "Under Pressure" - How fungi evade, exploit, and modulate cells of the innate immune system.Seminars in immunology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The fungus Cryptococcus neoformans is a major human pathogen with a remarkable intracellular survival strategy that includes exiting macrophages through non-lytic exocytosis (Vomocytosis) and transferring between macrophages (Dragotcytosis) by a mechanism that involves sequential events of non-lytic exocytosis and phagocytosis. Vomocytosis and Dragotcytosis are fungal driven processes, but their triggers are not understood. We hypothesized that the dynamics of Dragotcytosis could inherit the stochasticity of phagolysosome acidification and that Dragotcytosis was triggered by fungal cell stress. Consistent with this view, fungal cells involved in Dragotcytosis reside in phagolysosomes characterized by low pH and/or high oxidative stress. Using fluorescent microscopy, qPCR, live cell video microscopy, and fungal growth assays we found that the that mitigating pH or oxidative stress reduced Dragotcytosis frequency, whereas ROS susceptible mutants of C. neoformans underwent Dragotcytosis more frequently. Dragotcytosis initiation was linked to phagolysosomal pH, oxidative stresses, and macrophage polarization state. Dragotcytosis manifested stochastic dynamics thus paralleling the dynamics of phagosomal acidification, which correlated with the inhospitality of phagolysosomes in differently polarized macrophages. Hence, randomness in phagosomal acidification randomly created a population of inhospitable phagosomes where fungal cell stress triggered stochastic C. neoformans non-lytic exocytosis dynamics to escape a non-permissive intracellular macrophage environment.
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Registered trials
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