ArticleMycopathologia2013
Development of in vitro macrophage system to evaluate phagocytosis and intracellular fate of Penicillium marneffei conidia.
Article in Mycopathologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Talaromyces marneffei, Coccidioides species, and Paracoccidioides species-a systematic review to inform the World Health Organization priority list of fungal pathogens.Medical mycology · 2024Pooled it
- An unusual Toll/MyD88-mediatedFly · 2024Article
- Differential innate immune responses of human macrophages and bronchial epithelial cells againstmSphere · 2023Article
- Review
- Neglected mycobiome in HIV infection: Alterations, common fungal diseases and antifungal immunity.Frontiers in immunology · 2022Review
- Article
- Disseminated Coinfection byInfection and drug resistance · 2021Article
- Murine Macrophage Requires CD11b to RecognizeInfection and drug resistance · 2020Article
- Sixty Years from Segretain's Description: What Have We Learned and Should Learn About the Basic Mycology of Talaromyces marneffei?Mycopathologia · 2019Article
- Talaromycosis (Penicilliosis) Due to Talaromyces (Penicillium) marneffei: Insights into the Clinical Trends of a Major Fungal Disease 60 Years After the Discovery of the Pathogen.Mycopathologia · 2019Review
- Article
- Acute Penicillium marneffei infection stimulates host M1/M2a macrophages polarization in BALB/C mice.BMC microbiology · 2017Article
- Adaptation to macrophage killing byFuture science OA · 2017Review
- LungSAGE open medical case reports · 2017Article
- Detection of Talaromyces marneffei from Fresh Tissue of an Inhalational Murine Pulmonary Model Using Nested PCR.PloS one · 2016Article
- Galleria mellonella Larvae as an Infection Model for Penicillium marneffei.Mycopathologia · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Penicillium marneffei is a pathogenic fungus that can cause a life-threatening systemic mycosis in the immunocompromised hosts. We established the model for the phagocytosis of P. marneffei conidia by RAW264.7 murine macrophages and designated the fate of P. marneffei in RAW264.7 cells with respect to persistence, phagosome-lysosome-fusion. And we impaired the immune status of mouse and compared the fate and phagosome-lysosome-fusion of P. marneffei in immunocompetent and immunosuppressed mouse peritoneal macrophages cells. We found that conidia could germinate and survive in macrophages. Within 30 min and up to 2 h of heat-killed conidia internalization, the majority of all phagosome types were labeled for the EEA1 (endosomal markers) and LAMP-1 (lysosomal markers), respectively. But both the percentages of LAMP-1 and EEA1 that associated with live conidia were significantly lower than that with heat-killed conidia. Administration of cyclophosphamide resulted in a significant suppression of macrophages function (phagocytic and fungicidal) against P. marneffei that were not apparently seen. Our data provide the evidence that (i) intracellular conversion of P. marneffei conidia into yeast cells still could be observed in macrophages. (ii) Phagosomes containing live Penicillium marneffei conidia might inhibit the phagosome-lysosome-fusion and result to no acidification surrounding the organisms. (iii) Immunity impaired by cyclophosphamide could not influence the function, including phagocytosis, fungicidal activity and phagosome-lysosome-fusion, of macrophages against P. marneffei.
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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.