Intestinal Cell Tight Junctions Limit Invasion of Candida albicans through Active Penetration and Endocytosis in the Early Stages of the Interaction of the Fungus with the Intestinal Barrier

Autor: Frédéric Dalle, Coralie L'Ollivier, Gudrun Holland, Fabienne Bon, Michael Laue, Alain Bonnin, Marianne Goyer, Alicia Loiselet
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Cellular differentiation
Cell Lines
lcsh:Medicine
Yeast and Fungal Models
Pathology and Laboratory Medicine
Epithelium
Animal Cells
Candida albicans
Medicine and Health Sciences
Intestinal Mucosa
Internalization
lcsh:Science
media_common
Candida
Fungal Pathogens
Staining
Multidisciplinary
Secretory Pathway
Tight junction
Candidiasis
Cell Staining
Cell Differentiation
Corpus albicans
Endocytosis
Cell biology
Intestines
Medical Microbiology
Cell Processes
Host-Pathogen Interactions
Biological Cultures
Pathogens
Anatomy
Cellular Types
Research Article
media_common.quotation_subject
030106 microbiology
Mycology
Biology
Research and Analysis Methods
Microbiology
Tight Junctions
03 medical and health sciences
Model Organisms
Humans
Microbial Pathogens
lcsh:R
Organisms
Fungi
Biology and Life Sciences
Epithelial Cells
Cell Biology
biology.organism_classification
Yeast
Gastrointestinal Tract
030104 developmental biology
Biological Tissue
Caco-2
Specimen Preparation and Treatment
lcsh:Q
Caco-2 Cells
Digestive System
Developmental Biology
Zdroj: PLoS ONE, Vol 11, Iss 3, p e0149159 (2016)
PLoS ONE
ISSN: 1932-6203
Popis: C. albicans is a commensal yeast of the mucous membranes in healthy humans that can also cause disseminated candidiasis, mainly originating from the digestive tract, in vulnerable patients. It is necessary to understand the cellular and molecular mechanisms of the interaction of C. albicans with enterocytes to better understand the basis of commensalism and pathogenicity of the yeast and to improve the management of disseminated candidiasis. In this study, we investigated the kinetics of tight junction (TJ) formation in parallel with the invasion of C. albicans into the Caco-2 intestinal cell line. Using invasiveness assays on Caco-2 cells displaying pharmacologically altered TJ (i.e. differentiated epithelial cells treated with EGTA or patulin), we were able to demonstrate that TJ protect enterocytes against invasion of C. albicans. Moreover, treatment with a pharmacological inhibitor of endocytosis decreased invasion of the fungus into Caco-2 cells displaying altered TJ, suggesting that facilitating access of the yeast to the basolateral side of intestinal cells promotes endocytosis of C. albicans in its hyphal form. These data were supported by SEM observations of differentiated Caco-2 cells displaying altered TJ, which highlighted membrane protrusions engulfing C. albicans hyphae. We furthermore demonstrated that Als3, a hypha-specific C. albicans invasin, facilitates internalization of the fungus by active penetration and induced endocytosis by differentiated Caco-2 cells displaying altered TJ. However, our observations failed to demonstrate binding of Als3 to E-cadherin as the trigger mechanism of endocytosis of C. albicans into differentiated Caco-2 cells displaying altered TJ.
Databáze: OpenAIRE
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