Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity
The fungus Candida albicans colonizes the oral mucosal surface of 30–70% of healthy individuals. Due to local or systemic immunosuppression, this commensal fungus is able to proliferate resulting in oral disease, called oropharyngeal candidiasis (OPC). However, in healthy individuals C. albicans cau...
Main Authors: | , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Frontiers Media S.A.
2020-10-01
|
Series: | Frontiers in Immunology |
Subjects: | |
Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2020.555363/full |
id |
doaj-e41a89837fdc4dbab40e4eef1ac9414a |
---|---|
record_format |
Article |
spelling |
doaj-e41a89837fdc4dbab40e4eef1ac9414a2020-11-25T03:45:07ZengFrontiers Media S.A.Frontiers in Immunology1664-32242020-10-011110.3389/fimmu.2020.555363555363Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral CavityNicolas Millet0Nicolas Millet1Norma V. Solis2Norma V. Solis3Marc Swidergall4Marc Swidergall5Marc Swidergall6Division of Infectious Diseases, Harbor-UCLA Medical Center, Torrance, CA, United StatesInstitute for Infection and Immunity, The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA, United StatesDivision of Infectious Diseases, Harbor-UCLA Medical Center, Torrance, CA, United StatesInstitute for Infection and Immunity, The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA, United StatesDivision of Infectious Diseases, Harbor-UCLA Medical Center, Torrance, CA, United StatesInstitute for Infection and Immunity, The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA, United StatesDavid Geffen School of Medicine at UCLA, Los Angeles, CA, United StatesThe fungus Candida albicans colonizes the oral mucosal surface of 30–70% of healthy individuals. Due to local or systemic immunosuppression, this commensal fungus is able to proliferate resulting in oral disease, called oropharyngeal candidiasis (OPC). However, in healthy individuals C. albicans causes no harm. Unlike humans mice do not host C. albicans in their mycobiome. Thus, oral fungal challenge generates an acute immune response in a naive host. Therefore, we utilized C. albicans clinical isolates which are able to persist in the oral cavity without causing disease to analyze adaptive responses to oral fungal commensalism. We performed RNA sequencing to determine the transcriptional host response landscape during C. albicans colonization. Pathway analysis revealed an upregulation of adaptive host responses due to C. albicans oral persistence, including the upregulation of the immune network for IgA production. Fungal colonization increased cross-specific IgA levels in the saliva and the tongue, and IgA+ cells migrated to foci of fungal colonization. Binding of IgA prevented fungal epithelial adhesion and invasion resulting in a dampened proinflammatory epithelial response. Besides CD19+ CD138− B cells, plasmablasts, and plasma cells were enriched in the tongue of mice colonized with C. albicans suggesting a potential role of B lymphocytes during oral fungal colonization. B cell deficiency increased the oral fungal load without causing severe OPC. Thus, in the oral cavity B lymphocytes contribute to control commensal C. albicans carriage by secreting IgA at foci of colonization thereby preventing fungal dysbiosis.https://www.frontiersin.org/articles/10.3389/fimmu.2020.555363/fulloropharyngeal candidiasiscommensalismfungihost-pathogen interactionB cellantifungal immunity |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Nicolas Millet Nicolas Millet Norma V. Solis Norma V. Solis Marc Swidergall Marc Swidergall Marc Swidergall |
spellingShingle |
Nicolas Millet Nicolas Millet Norma V. Solis Norma V. Solis Marc Swidergall Marc Swidergall Marc Swidergall Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity Frontiers in Immunology oropharyngeal candidiasis commensalism fungi host-pathogen interaction B cell antifungal immunity |
author_facet |
Nicolas Millet Nicolas Millet Norma V. Solis Norma V. Solis Marc Swidergall Marc Swidergall Marc Swidergall |
author_sort |
Nicolas Millet |
title |
Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity |
title_short |
Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity |
title_full |
Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity |
title_fullStr |
Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity |
title_full_unstemmed |
Mucosal IgA Prevents Commensal Candida albicans Dysbiosis in the Oral Cavity |
title_sort |
mucosal iga prevents commensal candida albicans dysbiosis in the oral cavity |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Immunology |
issn |
1664-3224 |
publishDate |
2020-10-01 |
description |
The fungus Candida albicans colonizes the oral mucosal surface of 30–70% of healthy individuals. Due to local or systemic immunosuppression, this commensal fungus is able to proliferate resulting in oral disease, called oropharyngeal candidiasis (OPC). However, in healthy individuals C. albicans causes no harm. Unlike humans mice do not host C. albicans in their mycobiome. Thus, oral fungal challenge generates an acute immune response in a naive host. Therefore, we utilized C. albicans clinical isolates which are able to persist in the oral cavity without causing disease to analyze adaptive responses to oral fungal commensalism. We performed RNA sequencing to determine the transcriptional host response landscape during C. albicans colonization. Pathway analysis revealed an upregulation of adaptive host responses due to C. albicans oral persistence, including the upregulation of the immune network for IgA production. Fungal colonization increased cross-specific IgA levels in the saliva and the tongue, and IgA+ cells migrated to foci of fungal colonization. Binding of IgA prevented fungal epithelial adhesion and invasion resulting in a dampened proinflammatory epithelial response. Besides CD19+ CD138− B cells, plasmablasts, and plasma cells were enriched in the tongue of mice colonized with C. albicans suggesting a potential role of B lymphocytes during oral fungal colonization. B cell deficiency increased the oral fungal load without causing severe OPC. Thus, in the oral cavity B lymphocytes contribute to control commensal C. albicans carriage by secreting IgA at foci of colonization thereby preventing fungal dysbiosis. |
topic |
oropharyngeal candidiasis commensalism fungi host-pathogen interaction B cell antifungal immunity |
url |
https://www.frontiersin.org/articles/10.3389/fimmu.2020.555363/full |
work_keys_str_mv |
AT nicolasmillet mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity AT nicolasmillet mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity AT normavsolis mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity AT normavsolis mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity AT marcswidergall mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity AT marcswidergall mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity AT marcswidergall mucosaligapreventscommensalcandidaalbicansdysbiosisintheoralcavity |
_version_ |
1724511189216526336 |