Mucosal damage and neutropenia are required for Candida albicans dissemination.

Candida albicans fungemia in cancer patients is thought to develop from initial gastrointestinal (GI) colonization with subsequent translocation into the bloodstream after administration of chemotherapy. It is unclear what components of the innate immune system are necessary for preventing C. albica...

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Autores principales:	Andrew Y Koh, Julia R Köhler, Kathleen T Coggshall, Nico Van Rooijen, Gerald B Pier
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/d0e454124b28474ca0f936e4bf4e1546
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spelling	oai:doaj.org-article:d0e454124b28474ca0f936e4bf4e15462021-11-25T05:46:43ZMucosal damage and neutropenia are required for Candida albicans dissemination.1553-73661553-737410.1371/journal.ppat.0040035https://doaj.org/article/d0e454124b28474ca0f936e4bf4e15462008-02-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18282097/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Candida albicans fungemia in cancer patients is thought to develop from initial gastrointestinal (GI) colonization with subsequent translocation into the bloodstream after administration of chemotherapy. It is unclear what components of the innate immune system are necessary for preventing C. albicans dissemination from the GI tract, but we have hypothesized that both neutropenia and GI mucosal damage are critical for allowing widespread invasive C. albicans disease. We investigated these parameters in a mouse model of C. albicans GI colonization that led to systemic spread after administration of immunosuppression and mucosal damage. After depleting resident GI intestinal flora with antibiotic treatment and achieving stable GI colonization levels of C. albicans, it was determined that systemic chemotherapy with cyclophosphamide led to 100% mortality, whereas selective neutrophil depletion, macrophage depletion, lymphopenia or GI mucosal disruption alone resulted in no mortality. Selective neutrophil depletion combined with GI mucosal disruption led to disseminated fungal infection and 100% mortality ensued. GI translocation and dissemination by C. albicans was also dependent on the organism's ability to transform from the yeast to the hyphal form. This mouse model of GI colonization and fungemia is useful for studying factors of innate host immunity needed to prevent invasive C. albicans disease as well as identifying virulence factors that are necessary for fungal GI colonization and dissemination. The model may also prove valuable for evaluating therapies to control C. albicans infections.Andrew Y KohJulia R KöhlerKathleen T CoggshallNico Van RooijenGerald B PierPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 4, Iss 2, p e35 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Andrew Y Koh Julia R Köhler Kathleen T Coggshall Nico Van Rooijen Gerald B Pier Mucosal damage and neutropenia are required for Candida albicans dissemination.
description	Candida albicans fungemia in cancer patients is thought to develop from initial gastrointestinal (GI) colonization with subsequent translocation into the bloodstream after administration of chemotherapy. It is unclear what components of the innate immune system are necessary for preventing C. albicans dissemination from the GI tract, but we have hypothesized that both neutropenia and GI mucosal damage are critical for allowing widespread invasive C. albicans disease. We investigated these parameters in a mouse model of C. albicans GI colonization that led to systemic spread after administration of immunosuppression and mucosal damage. After depleting resident GI intestinal flora with antibiotic treatment and achieving stable GI colonization levels of C. albicans, it was determined that systemic chemotherapy with cyclophosphamide led to 100% mortality, whereas selective neutrophil depletion, macrophage depletion, lymphopenia or GI mucosal disruption alone resulted in no mortality. Selective neutrophil depletion combined with GI mucosal disruption led to disseminated fungal infection and 100% mortality ensued. GI translocation and dissemination by C. albicans was also dependent on the organism's ability to transform from the yeast to the hyphal form. This mouse model of GI colonization and fungemia is useful for studying factors of innate host immunity needed to prevent invasive C. albicans disease as well as identifying virulence factors that are necessary for fungal GI colonization and dissemination. The model may also prove valuable for evaluating therapies to control C. albicans infections.
format	article
author	Andrew Y Koh Julia R Köhler Kathleen T Coggshall Nico Van Rooijen Gerald B Pier
author_facet	Andrew Y Koh Julia R Köhler Kathleen T Coggshall Nico Van Rooijen Gerald B Pier
author_sort	Andrew Y Koh
title	Mucosal damage and neutropenia are required for Candida albicans dissemination.
title_short	Mucosal damage and neutropenia are required for Candida albicans dissemination.
title_full	Mucosal damage and neutropenia are required for Candida albicans dissemination.
title_fullStr	Mucosal damage and neutropenia are required for Candida albicans dissemination.
title_full_unstemmed	Mucosal damage and neutropenia are required for Candida albicans dissemination.
title_sort	mucosal damage and neutropenia are required for candida albicans dissemination.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/d0e454124b28474ca0f936e4bf4e1546
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Mucosal damage and neutropenia are required for Candida albicans dissemination.

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