Candida albicans: a model organism to study the role of micromycetes in the intestinal microbiota
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Titre | Candida albicans: a model organism to study the role of micromycetes in the intestinal microbiota |
Type de publication | Journal Article |
Year of Publication | 2018 |
Auteurs | Bonnin A, Dalle F |
Journal | BULLETIN DE L ACADEMIE NATIONALE DE MEDECINE |
Volume | 202 |
Pagination | 1401-1411 |
Date Published | SEP-OCT |
Type of Article | Article |
ISSN | 0001-4079 |
Mots-clés | Candida albicans, INTESTINAL MUCOSA, M CELLS, MYCOBIOTA, TIGHT-JUNCTIONS |
Résumé | Among micro-organisms that inhabit the gut, fungi represent a minor fraction, idenified as the mycobiota, and estimated at less than 0.1 % of the entire microbiota. Recent works suggest that modifications of the microbiota are involved in the pathogenesis of multiple diseases, including inflammatory bowel diseases, with increased proportions of Candida spp. and noticeably Candida albicans, a micromycete part of the normal gut flora in more than 50 % of healthy individuals, being reported. Therefore, C. albicans represents a model organism for the analysis of the role of the intestinal mycobiota. The intestinal epithelium is the first barrier during C. albicans interaction with the mucosa. Enterocytes grown in mature differentiated monolayers cannot internalize C. albicans by induced endocytosis, and the only mechanism of penetration into enterocytes is by active penetration of the fungus. In the present paper, we present results showing that endocytosis by enterocytes is restored upon alteration of tight junctions, that provide access to the basolateral side of the cells. We also show that C. albicans is able to use microfold cells (or M cells), a population of epithelial cells specialized in endocytosis of molecules or micro-organisms from the intestinal lumen, to invade the mucosa. These data provide a cellular basis for hypotheses involving the mycobiota in the pathogenesis of gut inflammation. They also contribute to a better understanding of the mechanisms involved at the early stages of invasive candidiasis with an intestinal portal of entry. |
DOI | 10.1016/S0001-4079(19)30206-7 |