ArticlePloS one2013
A mouse model for Candida glabrata hematogenous disseminated infection starting from the gut: evaluation of strains with different adhesion properties.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
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- Virulence assessment of six major pathogenic Candida species in the mouse model of invasive candidiasis caused by fungal translocation.Scientific reports · 2020Article
- The role of Lactobacillus species in the control of Candida via biotrophic interactions.Microbial cell (Graz, Austria) · 2019Review
- Divergent Approaches to Virulence inInternational journal of molecular sciences · 2019Review
- Induced Aberrant Organisms with Novel Ability to Protect Intestinal Integrity from Inflammation in an Animal Model.Nutrients · 2017Article
- Evolution of reduced co-activator dependence led to target expansion of a starvation response pathway.eLife · 2017Article
- Combination of Estrogen and Immunosuppressive Agents to Establish a Mouse Model of Candidiasis with Concurrent Oral and Vaginal Mucosal Infection.Mycopathologia · 2016Article
- Of mice, flies--and men? Comparing fungal infection models for large-scale screening efforts.Disease models & mechanisms · 2015Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adhesion to digestive mucosa is considered a crucial first step in the pathogenicity of invasive Candida infections. Candida glabrata disseminated infections predominantly start from the gut. A mouse model of disseminated infection starting from the gut was set up. Hematogenous dissemination was obtained after a low-protein diet followed by a regimen of cyclophosphamide-methotrexate and an oral inoculation of the yeasts via the drinking water. The liver was the first organ infected (day 7 post-infection), and lethality was 100% at day 21 post-infection. This new mouse model was used to compare the mortality rate and fungal burden in deep organs induced by 5 strains exhibiting different levels of adhesion to enterocyte Caco-2 cells, as determined in a test on 36 C. glabrata strains. In this model, no statistical difference of lethality was demonstrated between the strains, and fungal burden varied in kidneys and lungs but without correlation with the level of adhesion to enterocytes. Further studies using the model developed here allow analysis of the crossing of the digestive mucosa by yeasts, and help relate this to yet-poorly understood adhesion phenotypes.
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