ArticlePloS one2019
Oral Candida administration in a Clostridium difficile mouse model worsens disease severity but is attenuated by Bifidobacterium.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 65 citations in OpenAlex.
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- Impact of interkingdom microbial interactions in the vaginal tract.PLoS pathogens · 2024Article
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- Therapeutic Approach Targeting Gut Microbiome in Gastrointestinal Infectious Diseases.International journal of molecular sciences · 2023Review
- A prebiotic diet modulates the oral microbiome composition and results in the attenuation of oropharyngeal candidiasis in mice.Microbiology spectrum · 2023Article
- The Intricate Connection between Bacterial α-Diversity and Fungal Engraftment in the Human Gut of Healthy and Impaired Individuals as Studied Using the In Vitro SHIMEJournal of fungi (Basel, Switzerland) · 2023Article
- Pre-colonization with the fungusmSphere · 2023Article
- The leaky gut and the gut microbiome in sepsis - targets in research and treatment.Clinical science (London, England : 1979) · 2023Article
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- Regulatory effects of oral microbe on intestinal microbiota and the illness.Frontiers in cellular and infection microbiology · 2023Review
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- Analysis of Intestinal Mycobiota of Patients with Clostridioides difficile Infection among a Prospective Inpatient Cohort.Microbiology spectrum · 2022Article
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- Sepsis Encephalopathy Is Partly Mediated by miR370-3p-Induced Mitochondrial Injury but Attenuated by BAM15 in Cecal Ligation and Puncture Sepsis Male Mice.International journal of molecular sciences · 2022Article
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- Uremia-Induced Gut Barrier Defect in 5/6 Nephrectomized Mice Is Worsened byInternational journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gut fungi may influence the course of Clostridium difficile infection either positively or negatively for the host. Fungi are not prominent in the mouse gut, and C. albicans, the major human gastrointestinal commensal yeast, is in low abundance or absent in mice. Bifidobacterium is one of the probiotics that may attenuate the severity of C. difficile infection. Inflammatory synergy between C. albicans and C. difficile, in gut, may provide a state that more closely resembles human infection and be more suitable for testing probiotic effects. We performed fecal mycobiota analysis and administered C. albicans at 1 day prior to C. difficile dosing. Fecal eukaryotic 18S rDNA analysis demonstrated the presence of Ascomycota, specifically, Candida spp., after oral antibiotics, despite negative fecal fungal culture. C. albicans administration enhanced the severity of the C. difficile infection model as determined by mortality rate, weight loss, gut leakage (FITC-dextran assay), and serum and intestinal tissue cytokines. This occurred without increased fecal C. difficile or bacteremia, in comparison with C. difficile gavage alone. Candida lysate with C. difficile increased IL-8 production from HT-29 and Caco-2 human intestinal epithelial cell-lines. Bifidobacterium attenuated the disease severity of the C. difficile plus Candida model. The reduced severity was associated with decreased Candida burdens in feces. In conclusion, gut C. albicans worsened C. difficile infection, possibly through exacerbation of inflammation. Hence, a mouse model of Clostridium difficile infection with C. albicans present in the gut may better model the human patient condition. Gut fungal mycobiome investigation in patients with C. difficile is warranted and may suggest therapeutic targets.
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