ArticleVirulence2013
The role of Candida albicans AP-1 protein against host derived ROS in in vivo models of infection.
Article in Virulence, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 44 citations in OpenAlex.
- A roadmap to chemically reactive species: how diverse oxidants affectMicrobiology and molecular biology reviews : MMBR · 2025Review
- Shaker/Kv1 potassium channel SHK-1 protects against pathogen infection and oxidative stress in C. elegans.PLoS genetics · 2025Article
- Candida albicans pathways that protect against organic peroxides and lipid peroxidation.PLoS genetics · 2024Article
- Halofantrine Hydrochloride Acts as an Antioxidant Ability Inhibitor That Enhances Oxidative Stress Damage toAntioxidants (Basel, Switzerland) · 2024Article
- Alternative Non-Mammalian Animal and Cellular Methods for the Study of Host-Fungal Interactions.Journal of fungi (Basel, Switzerland) · 2023Review
- Oxidative stress response pathways in fungi.Cellular and molecular life sciences : CMLS · 2022Review
- Host Defense Mechanisms Induce Genome Instability Leading to Rapid Evolution in an Opportunistic Fungal Pathogen.Infection and immunity · 2022Article
- The impact of the Fungus-Host-Microbiota interplay upon Candida albicans infections: current knowledge and new perspectives.FEMS microbiology reviews · 2021Review
- Comprehensive genetic analysis of adhesin proteins and their role in virulence of Candida albicans.Genetics · 2021Article
- Review
- Virulence phenotypes result from interactions between pathogen ploidy and genetic background.Ecology and evolution · 2020Article
- A Novel Virulence Phenotype Rapidly AssessesmSphere · 2019Article
- Genetically Compromising Phospholipid Metabolism Limits Candida albicans' Virulence.Mycopathologia · 2019Article
- Review
- Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging.Antioxidants (Basel, Switzerland) · 2018Review
- The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions.Journal of visualized experiments : JoVE · 2017Article
- Stress Adaptation.Microbiology spectrum · 2017Review
- Caenorhabditis elegans as a model for understanding ROS function in physiology and disease.Redox biology · 2017Review
- Article
- The Mitochondrial GTPase Gem1 Contributes to the Cell Wall Stress Response and Invasive Growth ofFrontiers in microbiology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Candida albicans is a major fungal pathogen of humans, causing mucosal infections that are difficult to eliminate and systemic infections that are often lethal primarily due to defects in the host's innate status. Here we demonstrate the utility of Caenorhabditis elegans, a model host to study innate immunity, by exploring the role of reactive oxygen species (ROS) as a critical innate response against C. albicans infections. Much like a human host, the nematode's innate immune response is activated to produce ROS in response to fungal infection. We use the C. albicans cap1 mutant, which is susceptible to ROS, as a tool to dissect this physiological innate immune response and show that cap1 mutants fail to cause disease and death, except in bli-3 mutant worms that are unable to produce ROS because of a defective NADPH oxidase. We further validate the ROS-mediated host defense mechanism in mammalian phagocytes by demonstrating that chemical inhibition of the NADPH oxidase in cultured macrophages enables the otherwise susceptible cap1 mutant to resists ROS-mediated phagolysis. Loss of CAP1 confers minimal attenuation of virulence in a disseminated mouse model, suggesting that CAP1-independent mechanisms contribute to pathogen survival in vivo. Our findings underscore a central theme in the process of infection-the intricate balance between the virulence strategies employed by C. albicans and the host's innate immune system and validates C. elegans as a simple model host to dissect this balance at the molecular level.
Indexed as
Identifiers
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.