Abstract
Prior antibiotic treatment is a risk factor for Clostridioides difficile infection (CDI); the commensal gut microbiota plays a key role in determining host susceptibility to the disease. Previous studies demonstrate that the pre-colonization of mice with a commensal fungus, Candida albicans, protects against a lethal challenge with C. difficile spores. The results reported here demonstrate that the cecum contents of antibiotic-treated mice with C. albicans colonization contained different levels of several lipid species, including non-esterified, unsaturated long-chain fatty acids compared to non-C. albicans-colonized mice. Mice fed olive oil for one week and challenged with C. difficile spores showed enhanced survival compared to PBS-fed mice. The amount of olive oil administered was not sufficient to cause weight gain or to result in significant changes to the bacterial microbiota, in contrast to the effects of a high-fat diet. Furthermore, the direct exposure of C. difficile bacteria in laboratory culture to the unsaturated fatty acid oleic acid, the major fatty acid found in olive oil, reduced the transcription of genes encoding the toxins and reduced the survival of bacteria in the post-exponential phase. Therefore, the effects of C. albicans on the metabolite milieu contributed to the attenuation of C. difficile virulence.
Highlights
The opportunistic pathogenic fungus Candida albicans is the most common fungal colonizer of the human gastrointestinal tract [1,2,3,4]
To determine the effect of C. albicans colonization on the metabolite milieu of the intestinal tract, mice were treated with antibiotic to increase their susceptibility to Clostridioides difficile infection (CDI), but instead of receiving spores, the mice were sacrificed and the contents of the cecum were collected and rapidly frozen
The mice were rested for 20 days in smaller groups (4/cage with C. albicans-colonized mice separated from the non-colonized mice) with water lacking antibiotics
Summary
The opportunistic pathogenic fungus Candida albicans is the most common fungal colonizer of the human gastrointestinal tract [1,2,3,4]. C. albicans has been shown to have significant effects on bacterial population diversity after antibiotic treatment in a murine model [16], suggesting a significant role as a commensal. There is a lack of knowledge about the role fungi play during the bacterial infection of the gastrointestinal tract. Clostridioides difficile is an anaerobic, Gram-positive, spore-forming, and toxin-producing bacterial pathogen able to cause mild (antibiotic-associated diarrhea) [17,18] to severe, potentially fatal, gastrointestinal disease (pseudomembranous colitis, toxic megacolon) [19,20,21,22] primarily in those who are elderly, have been hospitalized, and/or received a course of broad-spectrum antibiotics [23,24]. Antibiotic treatment and Clostridioides difficile infection (CDI) are inextricably linked and the disease has been labeled as an urgent public health concern by the United States White House’s
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