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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| 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. |
| doi_str_mv | 10.1371/journal.ppat.0040035 |
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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.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.0040035</identifier><identifier>PMID: 18282097</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Anti-Bacterial Agents - pharmacology ; Bacterial Translocation - drug effects ; Cancer ; Cancer therapies ; Candida albicans - drug effects ; Candida albicans - pathogenicity ; Candidiasis - drug therapy ; Candidiasis - immunology ; Candidiasis - microbiology ; Chemotherapy ; Cyclophosphamide - therapeutic use ; Disease Models, Animal ; Experiments ; Female ; Fungal infections ; Fungi ; Gastrointestinal Tract - microbiology ; Gastrointestinal Tract - pathology ; Gene Silencing ; Homo (human) ; Immunology ; Immunosuppression Therapy ; Infectious Diseases ; Liver ; Longevity - drug effects ; Mice ; Mice, Inbred C3H ; Mice, Knockout ; Mortality ; Mucous Membrane - drug effects ; Mucous Membrane - microbiology ; Mucous Membrane - pathology ; Mus (mouse) ; Neutropenia - chemically induced ; Neutropenia - microbiology ; Neutropenia - pathology ; Oncology ; Spleen ; Yeast and Fungi</subject><ispartof>PLoS pathogens, 2008-02, Vol.4 (2), p.e35</ispartof><rights>2008 Koh et al. 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 credited: Koh AY, Köhler JR, Coggshall KT, Van Rooijen N, Pier GB (2008) Mucosal Damage and Neutropenia Are Required for Candida albicans Dissemination . 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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.</description><subject>Animals</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Bacterial Translocation - drug effects</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Candida albicans - drug effects</subject><subject>Candida albicans - pathogenicity</subject><subject>Candidiasis - drug therapy</subject><subject>Candidiasis - immunology</subject><subject>Candidiasis - microbiology</subject><subject>Chemotherapy</subject><subject>Cyclophosphamide - therapeutic use</subject><subject>Disease Models, Animal</subject><subject>Experiments</subject><subject>Female</subject><subject>Fungal infections</subject><subject>Fungi</subject><subject>Gastrointestinal Tract - microbiology</subject><subject>Gastrointestinal Tract - pathology</subject><subject>Gene Silencing</subject><subject>Homo (human)</subject><subject>Immunology</subject><subject>Immunosuppression Therapy</subject><subject>Infectious Diseases</subject><subject>Liver</subject><subject>Longevity - 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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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>18282097</pmid><doi>10.1371/journal.ppat.0040035</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Bacterial Agents - pharmacology Bacterial Translocation - drug effects Cancer Cancer therapies Candida albicans - drug effects Candida albicans - pathogenicity Candidiasis - drug therapy Candidiasis - immunology Candidiasis - microbiology Chemotherapy Cyclophosphamide - therapeutic use Disease Models, Animal Experiments Female Fungal infections Fungi Gastrointestinal Tract - microbiology Gastrointestinal Tract - pathology Gene Silencing Homo (human) Immunology Immunosuppression Therapy Infectious Diseases Liver Longevity - drug effects Mice Mice, Inbred C3H Mice, Knockout Mortality Mucous Membrane - drug effects Mucous Membrane - microbiology Mucous Membrane - pathology Mus (mouse) Neutropenia - chemically induced Neutropenia - microbiology Neutropenia - pathology Oncology Spleen Yeast and Fungi |
| title | Mucosal damage and neutropenia are required for Candida albicans dissemination |
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