ArticleJournal of immunology research2015
Experimental autoimmune encephalomyelitis development is aggravated by Candida albicans infection.
Article in Journal of immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Exploring the mycobiota in multiple sclerosis: its influence on disease development and progression.Frontiers in immunology · 2025Article
- Contribution of CNS and extra-CNS infections to neurodegeneration: a narrative review.Journal of neuroinflammation · 2024Review
- The fungal gut microbiota in pediatric-onset multiple sclerosis.Frontiers in microbiology · 2024Article
- Systemic Infection by Non-Journal of fungi (Basel, Switzerland) · 2022Article
- Curdlan, a Microbial β-Glucan, Has Contrasting Effects on Autoimmune and Viral Models of Multiple Sclerosis.Frontiers in cellular and infection microbiology · 2022Article
- The roles of fungus in CNS autoimmune and neurodegeneration disorders.Frontiers in immunology · 2022Review
- Article
- Oral Colonization by Candida Species in Patients with Multiple Sclerosis.Mycopathologia · 2020Article
- Animal experimentation in transgenesis: evaluating course design in large classrooms.FEBS open bio · 2020Article
- Review
- Differential Behavior of Non-Frontiers in microbiology · 2018Article
- The Multibiome: The Intestinal Ecosystem's Influence on Immune Homeostasis, Health, and Disease.EBioMedicine · 2016Review
- Tolerogenic Vaccination with MOG/VitD Overcomes Aggravating Effect of C. albicans in Experimental Encephalomyelitis.CNS neuroscience & therapeutics · 2016Article
- Evaluation of APR1 Gene Expression in Candida albicans Strains Isolated From Patients With Multiple Sclerosis.Jundishapur journal of microbiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an inflammatory/autoimmune disease of the central nervous system (CNS) mainly mediated by myelin specific T cells. It is widely believed that environmental factors, including fungal infections, contribute to disease induction or evolution. Even though Candida infection among MS patients has been described, the participation of this fungus in this pathology is not clear. The purpose of this work was to evaluate the effect of a Candida albicans infection on experimental autoimmune encephalomyelitis (EAE) that is a widely accepted model to study MS. Female C57BL/6 mice were infected with C. albicans and 3 days later, animals were submitted to EAE induction by immunization with myelin oligodendrocyte glycoprotein. Previous infection increased the clinical score and also the body weight loss. EAE aggravation was associated with expansion of peripheral CD4(+) T cells and production of high levels of TNF-α, IFN-γ IL-6, and IL-17 by spleen and CNS cells. In addition to yeast and hyphae, fungus specific T cells were found in the CNS. These findings suggest that C. albicans infection before EAE induction aggravates EAE, and possibly MS, mainly by CNS dissemination and local induction of encephalitogenic cytokines. Peripheral production of encephalitogenic cytokines could also contribute to disease aggravation.
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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.