IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa

Mucosal infections with Candida albicans belong to the most frequent forms of fungal diseases. Host protection is conferred by cellular immunity; however, the induction of antifungal immunity is not well understood. Using a mouse model of oropharyngeal candidiasis (OPC) we show that interleukin-1 re...

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Main Authors:	Altmeier, Simon, Toska, Albulena, Sparber, Florian, Teijeira, Alvaro, Halin, Cornelia, LeibundGut-Landmann, Salomé
Format:	Online
Language:	English
Published:	Public Library of Science 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5025078/

id	pubmed-5025078
recordtype	oai_dc
spelling	pubmed-50250782016-09-27 IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa Altmeier, Simon Toska, Albulena Sparber, Florian Teijeira, Alvaro Halin, Cornelia LeibundGut-Landmann, Salomé Research Article Mucosal infections with Candida albicans belong to the most frequent forms of fungal diseases. Host protection is conferred by cellular immunity; however, the induction of antifungal immunity is not well understood. Using a mouse model of oropharyngeal candidiasis (OPC) we show that interleukin-1 receptor (IL-1R) signaling is critical for fungal control at the onset of infection through its impact on neutrophils at two levels. We demonstrate that both the recruitment of circulating neutrophils to the site of infection and the mobilization of newly generated neutrophils from the bone marrow depended on IL-1R. Consistently, IL-1R-deficient mice displayed impaired chemokine production at the site of infection and defective secretion of granulocyte colony-stimulating factor (G-CSF) in the circulation in response to C. albicans. Strikingly, endothelial cells were identified as the primary cellular source of G-CSF during OPC, which responded to IL-1α that was released from keratinocytes in the infected tissue. The IL-1-dependent crosstalk between two different cellular subsets of the nonhematopoietic compartment was confirmed in vitro using a novel murine tongue-derived keratinocyte cell line and an established endothelial cell line. These data establish a new link between IL-1 and granulopoiesis in the context of fungal infection. Together, we identified two complementary mechanisms coordinating the neutrophil response in the oral mucosa, which is critical for preventing fungal growth and dissemination, and thus protects the host from disease. Public Library of Science 2016-09-15 /pmc/articles/PMC5025078/ /pubmed/27632536 http://dx.doi.org/10.1371/journal.ppat.1005882 Text en © 2016 Altmeier et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Altmeier, Simon Toska, Albulena Sparber, Florian Teijeira, Alvaro Halin, Cornelia LeibundGut-Landmann, Salomé
spellingShingle	Altmeier, Simon Toska, Albulena Sparber, Florian Teijeira, Alvaro Halin, Cornelia LeibundGut-Landmann, Salomé IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
author_facet	Altmeier, Simon Toska, Albulena Sparber, Florian Teijeira, Alvaro Halin, Cornelia LeibundGut-Landmann, Salomé
author_sort	Altmeier, Simon
title	IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
title_short	IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
title_full	IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
title_fullStr	IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
title_full_unstemmed	IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
title_sort	il-1 coordinates the neutrophil response to c. albicans in the oral mucosa
description	Mucosal infections with Candida albicans belong to the most frequent forms of fungal diseases. Host protection is conferred by cellular immunity; however, the induction of antifungal immunity is not well understood. Using a mouse model of oropharyngeal candidiasis (OPC) we show that interleukin-1 receptor (IL-1R) signaling is critical for fungal control at the onset of infection through its impact on neutrophils at two levels. We demonstrate that both the recruitment of circulating neutrophils to the site of infection and the mobilization of newly generated neutrophils from the bone marrow depended on IL-1R. Consistently, IL-1R-deficient mice displayed impaired chemokine production at the site of infection and defective secretion of granulocyte colony-stimulating factor (G-CSF) in the circulation in response to C. albicans. Strikingly, endothelial cells were identified as the primary cellular source of G-CSF during OPC, which responded to IL-1α that was released from keratinocytes in the infected tissue. The IL-1-dependent crosstalk between two different cellular subsets of the nonhematopoietic compartment was confirmed in vitro using a novel murine tongue-derived keratinocyte cell line and an established endothelial cell line. These data establish a new link between IL-1 and granulopoiesis in the context of fungal infection. Together, we identified two complementary mechanisms coordinating the neutrophil response in the oral mucosa, which is critical for preventing fungal growth and dissemination, and thus protects the host from disease.
publisher	Public Library of Science
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5025078/
_version_	1613652924451258368

IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa

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