ArticleInfection and immunity2010
Conidia but not yeast cells of the fungal pathogen Histoplasma capsulatum trigger a type I interferon innate immune response in murine macrophages.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Dectin-1 stimulation promotes a distinct inflammatory signature in the setting of HIV-infection and aging.Aging · 2023Article
- Detection of Cytokines and Collectins in Bronchoalveolar Fluid Samples of Patients Infected withJournal of fungi (Basel, Switzerland) · 2021Article
- Epidemiology of epizootic lymphangitis of carthorses in northern Ethiopia using conventional diagnostic methods and nested polymerase chain reaction.BMC veterinary research · 2020Article
- Type I Interferons Ameliorate Zinc Intoxication of Candida glabrata by Macrophages and Promote Fungal Immune Evasion.iScience · 2020Article
- A transcriptional signature accurately identifies Aspergillus Infection across healthy and immunosuppressed states.Translational research : the journal of laboratory and clinical medicine · 2020Article
- Sensing the heat and the host: Virulence determinants ofVirulence · 2019Review
- Dimorphism and Dissemination ofThe American journal of tropical medicine and hygiene · 2019Article
- A novel myeloid cell in murine spleen defined through gene profiling.Journal of cellular and molecular medicine · 2019Article
- Helper T-cell responses and pulmonary fungal infections.Immunology · 2018Review
- Article
- Clash of the Cytokine Titans: counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses.Cellular & molecular immunology · 2017Review
- CD103+ Conventional Dendritic Cells Are Critical for TLR7/9-Dependent Host Defense against Histoplasma capsulatum, an Endemic Fungal Pathogen of Humans.PLoS pathogens · 2016Article
- Type I IFN Induction via Poly-ICLC Protects Mice against Cryptococcosis.PLoS pathogens · 2015Article
- Induction of caspase-11 by aspartyl proteinases of Candida albicans and implication in promoting inflammatory response.Infection and immunity · 2015Article
- Type I interferons in infectious disease.Nature reviews. Immunology · 2015Review
- Article
- Beneficial innate signaling interference for antibacterial responses by a Toll-like receptor-mediated enhancement of the MKP-IRF3 axis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Comparative transcriptomics of infectious spores from the fungal pathogen Histoplasma capsulatum reveals a core set of transcripts that specify infectious and pathogenic states.Eukaryotic cell · 2013Article
- Role of type I interferons in inflammasome activation, cell death, and disease during microbial infection.Frontiers in cellular and infection microbiology · 2013Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Histoplasma capsulatum is the most common cause of fungal respiratory infections and can lead to progressive disseminated infections, particularly in immunocompromised patients. Infection occurs upon inhalation of the aerosolized spores, known as conidia. Once inside the host, conidia are phagocytosed by alveolar macrophages. The conidia subsequently germinate and produce a budding yeast-like form that colonizes host macrophages and can disseminate throughout host organs and tissues. Even though conidia are the predominant infectious particle for H. capsulatum and are the first cell type encountered by the host during infection, very little is known at a molecular level about conidia or about their interaction with cells of the host immune system. We examined the interaction between conidia and host cells in a murine bone-marrow-derived macrophage model of infection. We used whole-genome expression profiling and quantitative reverse transcription-PCR (qRT-PCR) to monitor the macrophage signaling pathways that are modulated during infection with conidia. Our analysis revealed that type I interferon (IFN)-responsive genes and the beta type I IFN (IFN-beta) were induced in macrophages during infection with H. capsulatum conidia but not H. capsulatum yeast cells. Further analysis revealed that the type I IFN signature induced in macrophages in response to conidia is independent of Toll-like receptor (TLR) signaling and the cytosolic RNA sensor MAVS but is dependent on the transcription factor interferon regulatory factor 3 (IRF3). Interestingly, H. capsulatum growth was restricted in mice lacking the type I IFN receptor, indicating that an intact host type I IFN response is required for full virulence of H. capsulatum in mice.
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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.