Candida albicans-Epithelial Interactions: Dissecting the Roles of Active Penetration, Induced Endocytosis and Host Factors on the Infection Process

Wächtler, Betty; Citiulo, Francesco; Jablonowski, Nadja; Förster, Stephanie; Dalle, Frederic; Schaller, Martin; Wilson, Duncan; Hube, Bernhard

doi:10.1371/journal.pone.0036952

Cited by 250Antifungal resistance and susceptibilityFungal and yeast genetics researchFungal Infections and Studies

Candida albicans-Epithelial Interactions: Dissecting the Roles of Active Penetration, Induced Endocytosis and Host Factors on the Infection Process

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Wächtler, Betty, Citiulo, Francesco, Jablonowski, Nadja, Förster, Stephanie, Dalle, Frederic, Schaller, Martin, Wilson, Duncan, Hube, Bernhard·2012·PLoS ONE

DOI 10.1371/journal.pone.0036952PMC PMC3351431

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Abstract

Candida albicans frequently causes superficial infections by invading and damaging epithelial cells, but may also cause systemic infections by penetrating through epithelial barriers. C. albicans is a remarkable pathogen because it can invade epithelial cells via two distinct mechanisms: induced endocytosis, analogous to facultative intracellular enteropathogenic bacteria, and active penetration, similar to plant pathogenic fungi. Here we investigated the contributions of the two invasion routes of C. albicans to epithelial invasion. Using selective cellular inhibition approaches and differential fluorescence microscopy, we demonstrate that induced endocytosis contributes considerably to the early time points of invasion, while active penetration represents the dominant epithelial invasion route. Although induced endocytosis depends mainly on Als3-E-cadherin interactions, we observed E-cadherin independent induced endocytosis. Finally, we provide evidence of a protective role for serum factors in oral infection: human serum strongly inhibited C. albicans adhesion to, invasion and damage of oral epithelial cells.

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Als3 is required for both induced endocytosis and active penetration.
“This result is in contrast to what has been found for Als3, which is required for both induced endocytosis and active penetration [29], and provides a likely explanation for why Hyr1 is dispensable for induction of epithelial cell damage.”
From Candida albicans stimulates formation of a multi-receptor complex that mediates epithelial cell invasion during oropharyngeal infection (2023) · cites this paper as [29]
The Results section, under “Relative Contributions of Active Penetration, Induced Endocytosis and C. Albicans Invasins to Epithelial Invasion,” concludes that Als3 plays major roles in both processes. But deletion reduced rather than eliminated invasion under either condition, and killed als3Δ hyphae still underwent some induced endocytosis. The paper supports Als3 as important to both routes, not strictly required for either. (LLM, conf=0.88)
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Authors: Wächtler, B., Citiulo, F., Jablonowski, N., Förster, S., Dalle, F., Schaller, M., Wilson, D., & Hube, B.
Affiliations: Leibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) (DE)
University of Tübingen (DE)
Corresponding author: Hube, Bernhard
ORCID: Citiulo, Francesco
Schaller, Martin
Wilson, Duncan
Hube, Bernhard
Venue: PLoS ONE
Publisher: Public Library of Science (PLoS)
Published: 2012-05-14
Volume: 7
Issue: 5
Pages: e36952
ISSN: 1932-6203 (ISSN-L)
DOI: 10.1371/journal.pone.0036952
PMC: PMC3351431
OpenAlex: W1995203663
Cited by: 250
References: 45
Citations by year: 2026: 11 · 2025: 19 · 2024: 19 · 2023: 29 · 2022: 23 · 2021: 25 · 2020: 21 · 2019: 15 · 2018: 19 · 2017: 17 · 2016: 12 · 2015: 11 · 2014: 15 · 2013: 10 · 2012: 4
FWCI: 8.87
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: PLoS ONE (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Aberdeen University Research Archive (Aberdeen University) (submittedVersion)
HAL (submittedVersion, other-oa)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders: Deutsche Forschungsgemeinschaft (Hu528/10, SPP1160)
Bundesministerium für Bildung und Forschung (0315901B)
Topics: Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
Keywords: Candida albicans, epithelial invasion, ALS3, E-cadherin, oral epithelial cells, serum factors, fungal adhesion, host-pathogen interaction, oral candidiasis
MeSH terms: Blood Physiological Phenomena, Candida albicans, Candidiasis, Oral, Cell Adhesion, Cell Line, Endocytosis, Epithelial Cells, Fungal Proteins, Humans, Mouth Mucosa, Cadherins, Microscopy, Electron, Transmission, Host-Pathogen Interactions

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Candida albicans-Epithelial Interactions: Dissecting the Roles of Active Penetration, Induced Endocytosis and Host Factors on the Infection Process

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