ReviewThe FEBS journal2016
Histoplasma capsulatum surmounts obstacles to intracellular pathogenesis.
Review in The FEBS journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 68 citations in OpenAlex.
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Tissue distribution of Histoplasma capsulatum in deceased people living with HIV assessed by minimally invasive tissue sampling: An autopsy-based case series in the Brazilian Amazon.PLoS neglected tropical diseases · 2026Observational
- Macrophage phagocytosis ofmBio · 2026Article
- The Rpd3 histone deacetylase is a critical regulator of temperature-mediated morphogenesis and virulence in the human fungal pathogen Histoplasma.PLoS biology · 2026Article
- Adaptive metabolic strategies of intracellular bacterial pathogens.Frontiers in microbiology · 2026Review
- A roadmap to chemically reactive species: how diverse oxidants affectMicrobiology and molecular biology reviews : MMBR · 2025Review
- 125I inhibits the progression of cervical cancer by upregulating the HSF1/PU.1/SYK signaling pathway and consequently enhancing the apoptotic response mediated by ROS/USP7/P53.Scientific reports · 2025Article
- Signaling Pathways Regulating Dimorphism in Medically Relevant Fungal Species.Pathogens (Basel, Switzerland) · 2025Review
- Genotypic diversity, virulence, and molecular genetic tools inMicrobiology and molecular biology reviews : MMBR · 2024Review
- Influence of Zinc onJournal of fungi (Basel, Switzerland) · 2024Article
- Unveiling the menace: a thorough review of potential pandemic fungal disease.Frontiers in fungal biology · 2024Review
- Common virulence factors betweenCurrent research in microbial sciences · 2024Review
- Antifungal Activity of Chitosan againstJournal of fungi (Basel, Switzerland) · 2023Article
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- Endemic mycoses in children in North America: a review of radiologic findings.Pediatric radiology · 2023Review
- Comparative Genomics ofJournal of fungi (Basel, Switzerland) · 2023Article
- Antifungal Susceptibility Testing and Drug Discovery in the Dimorphic Fungus Histoplasma Capsulatum.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Pathogenicity & virulence ofVirulence · 2022Review
- Genome-scale CRISPR screening reveals that C3aR signaling is critical for rapid capture of fungi by macrophages.PLoS pathogens · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The fungal pathogen Histoplasma capsulatum causes respiratory and disseminated disease, even in immunocompetent hosts. In contrast to opportunistic pathogens, which are readily controlled by phagocytic cells, H. capsulatum yeasts are able to infect macrophages, survive antimicrobial defenses, and proliferate as an intracellular pathogen. In this review, we discuss some of the molecular mechanisms that enable H. capsulatum yeasts to overcome obstacles to intracellular pathogenesis. H. capsulatum yeasts gain refuge from extracellular obstacles such as antimicrobial lung surfactant proteins by engaging the β-integrin family of phagocytic receptors to promote entry into macrophages. In addition, H. capsulatum yeasts conceal immunostimulatory β-glucans to avoid triggering signaling receptors such as the β-glucan receptor Dectin-1. H. capsulatum yeasts counteract phagocyte-produced reactive oxygen species by expression of oxidative stress defense enzymes including an extracellular superoxide dismutase and an extracellular catalase. Within the phagosome, H. capsulatum yeasts block phagosome acidification, acquire essential metals such as iron and zinc, and utilize de novo biosynthesis pathways to overcome nutritional limitations. These mechanisms explain how H. capsulatum yeasts avoid and negate macrophage defense strategies and establish a hospitable intracellular niche, making H. capsulatum a successful intracellular pathogen of macrophages.
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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.