ArticleInfection and immunity2011
The interaction between Candida krusei and murine macrophages results in multiple outcomes, including intracellular survival and escape from killing.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- Elements of dissemination in cryptococcosis.mBio · 2024Review
- Propulsive cell entry diverts pathogens from immune degradation by remodeling the phagocytic synapse.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Fungal mechanisms of intracellular survival: what can we learn from bacterial pathogens?Infection and immunity · 2023Review
- Propulsive cell entry diverts pathogens from immune degradation by remodeling the phagocytic synapse.bioRxiv : the preprint server for biology · 2023Article
- Non-Journal of fungi (Basel, Switzerland) · 2022Review
- Article
- In vitro infection models to study fungal-host interactions.FEMS microbiology reviews · 2021Review
- Fungal immunity and pathogenesis in mammals versus the invertebrate model organism Galleria mellonella.Pathogens and disease · 2021Review
- Article
- AJournal of fungi (Basel, Switzerland) · 2021Article
- Viral infection triggers interferon-induced expulsion of live Cryptococcus neoformans by macrophages.PLoS pathogens · 2020Article
- Article
- Current Aspects in the Biology, Pathogeny, and Treatment ofInfection and drug resistance · 2020Review
- Early Interaction of Alternaria infectoria Conidia with Macrophages.Mycopathologia · 2019Article
- The critical role of Dectin-1 in host controlling systemicAmerican journal of translational research · 2019Article
- Article
- Differential Behavior of Non-Frontiers in microbiology · 2018Article
- Modelling the host-pathogen interactions of macrophages andJournal of the Royal Society, Interface · 2017Article
- Control of Phagocytosis by Microbial Pathogens.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida krusei is a fungal pathogen of interest for the scientific community for its intrinsic resistance to fluconazole. Little is known about the interaction of this yeast with host immune cells. In this work, we have characterized the outcome of the interaction between C. krusei and murine macrophages. Once C. krusei was internalized, we observed different phenomena. In a macrophage-like cell line, C. krusei survived in a significant number of macrophages and induced filamentation and macrophage explosion. Phagocytosis of C. krusei led to actin polymerization around the yeast cells at the site of entry. Fluorescent specific staining with anti-Lamp1 and LysoTracker indicated that after fungal internalization, there was a phagolysosome maturation defect, a phenomenon that was more efficient when the macrophages phagocytosed killed yeast cells. Using cell line macrophages, we also observed macrophage fusion after cell division. When we used primary resident peritoneal macrophages in addition to macrophage explosion, we also observed a strong chemotaxis of uninfected macrophages to regions where C. krusei-infected macrophages were present. We also noticed yeast transfer phenomena between infected macrophages. Primary macrophages inhibited pseudohypha elongation more efficiently than the macrophage-like cell line, suggesting that C. krusei infection was better controlled by the former macrophages. Primary macrophages induced more tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) than the macrophage-like cell line. Our results demonstrate that C. krusei can exploit the macrophages for replication, although other different outcomes are also possible, indicating that the interaction of this pathogen with phagocytic cells is very complex and regulated by multiple factors.
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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.