ArticleThe Journal of infectious diseases2014
Exacerbation of invasive Candida albicans infection by commensal bacteria or a glycolipid through IFN-γ produced in part by iNKT cells.
Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Commensal bacterial glycosylation at the interface of host-bacteria interactions.Gut microbes · 2025Review
- Epidemiology and outcomes of Candida-associated osteoarticular infections: A multicentre retrospective study from Turkey.Medical mycology · 2025Article
- LncRNA: A Potential Target for Host-Directed Therapy ofPharmaceutics · 2022Review
- Recombinant phage displaying ToAP2D peptide with antifungal activity againstFrontiers in pharmacology · 2022Article
- Type I Natural Killer T Cells as Key Regulators of the Immune Response to Infectious Diseases.Clinical microbiology reviews · 2021Review
- Article
- Single and Repeated Episodes ofFrontiers in microbiology · 2021Article
- Cryptococcus gattii alters immunostimulatory potential in response to the environment.PloS one · 2019Article
- Mouse LIMR3/CD300f is a negative regulator of the antimicrobial activity of neutrophils.Scientific reports · 2018Article
- Functions of CD1d-Restricted Invariant Natural Killer T Cells in Antimicrobial Immunity and Potential Applications for Infection Control.Frontiers in immunology · 2018Review
- An In vitro Comparative Evaluation of Disinfectants on Standard and Clinical Microbial Strains on Heat Cure Resins.Journal of clinical and diagnostic research : JCDR · 2017Article
- Novel nanoscale bacteriophage-based single-domain antibodies for the therapy of systemic infection caused by Candida albicans.Scientific reports · 2016Article
- New insights into innate immune control of systemic candidiasis.Medical mycology · 2014Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe commensal yeast Candida albicans is a major cause of invasive fungal infections. Despite treatment with antifungal agents, the mortality rate attributed to these types of infection is high. Although numerous cases have been reported regarding a poor outcome for patients with bacterial and C. albicans coinfection, the mechanisms by which the coinfecting bacteria exacerbate the C. albicans infection remain elusive. METHODS AND
resultsWe evaluated how glycolipid-mediated activation of invariant natural killer T (iNKT) cells affects the clearance of C. albicans. Surprisingly, C. albicans-infected, glycolipid-treated mice exhibited significantly lower survival rates, increased fungal burden, and higher interleukin (IL)-6 production in the kidneys compared with control mice. Glycolipid-induced exacerbation of C. albicans infection was not observed in interferon-gamma knockout (IFN-γKO) mice. In the C. albicans-infected, glycolipid-treated mice, the number of neutrophils in the blood and bone marrow dramatically decreased in an IFN-γ-dependent manner. Furthermore, mice that were coinfected with C. albicans and nonfermentative gram-negative commensal bacteria exhibited increased fungal burden and inflammatory cytokine production in the kidneys that were dependent on IFN-γ and iNKT cells.
conclusionsOur results indicate that coinfecting commensal bacteria exacerbate C. albicans infection through IFN-γ produced, in part, by iNKT cells.
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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.