author_facet Miura, Koshiro
Rikihisa, Yasuko
Miura, Koshiro
Rikihisa, Yasuko
author Miura, Koshiro
Rikihisa, Yasuko
spellingShingle Miura, Koshiro
Rikihisa, Yasuko
Infection and Immunity
Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
Infectious Diseases
Immunology
Microbiology
Parasitology
author_sort miura, koshiro
spelling Miura, Koshiro Rikihisa, Yasuko 0019-9567 1098-5522 American Society for Microbiology Infectious Diseases Immunology Microbiology Parasitology http://dx.doi.org/10.1128/iai.00979-08 <jats:title>ABSTRACT</jats:title><jats:p>Infection of humans with<jats:italic>Ehrlichia chaffeensis</jats:italic>, the etiologic agent of human monocytic ehrlichiosis, can cause hepatitis of various levels of severity. When the three human isolates of<jats:italic>E. chaffeensis</jats:italic>, each belonging to a different genogroup, are inoculated into severe combined immunodeficiency mice, the order of severity of clinical signs and bacterial burden detected in the liver is as follows (from greatest to least severity and highest to lowest burden): strain Wakulla, followed by strain Liberty, followed by strain Arkansas. In this article, we used microarray analysis to define transcriptional profiles characteristic of the histopathological features in the mouse liver. Cytokine and chemokine profiles and their receptor profiles were strikingly different among the three strains of<jats:italic>E. chaffeensis</jats:italic>: gamma interferon, CCL5, CXCL1, CXCL2, CXCL7, CXCL9, interleukin 2 receptor gamma (IL2Rγ), IL21R, CCR2, and CXCR6 were highly upregulated with strain Arkansas; and tumor necrosis factor (TNF), CCL2, CCL3, CCL5, CCL6, CCL12, CCL20, CXCL2, CXCL7, CXCL9, CXCL13, TNF receptor superfamily 9 (TNFRSF9), TNFRSF13β, IL1R2, IL2Rγ, IL20Rβ, IL21R, CCR1, CCR2, and CXCR4 were highly upregulated with strain Wakulla. With strain Liberty, only CXCL13 was highly upregulated, and IL13Rα2 was downregulated. In livers infected with the Arkansas strain, monocytes/macrophages and NK cells were enriched in the granulomas and an increase in NK cell marker mRNAs was detected. Livers infected with the Wakulla strain displayed infiltration of significantly more neutrophils and an increase in neutrophil marker mRNAs. Genes commonly upregulated in liver tissue infected with the three strains are other host innate immune and inflammatory response genes, including those encoding several acute-phase proteins. Genes downregulated commonly are related to host physiologic functions. The results suggest that marked modulation of host cytokine and chemokine profiles by<jats:italic>E. chaffeensis</jats:italic>strains underlies the distinct host liver disease.</jats:p> Liver Transcriptome Profiles Associated with Strain-Specific<i>Ehrlichia chaffeensis</i>-Induced Hepatitis in SCID Mice Infection and Immunity
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series Infection and Immunity
source_id 49
title Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_unstemmed Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_full Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_fullStr Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_full_unstemmed Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_short Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_sort liver transcriptome profiles associated with strain-specific<i>ehrlichia chaffeensis</i>-induced hepatitis in scid mice
topic Infectious Diseases
Immunology
Microbiology
Parasitology
url http://dx.doi.org/10.1128/iai.00979-08
publishDate 2009
physical 245-254
description <jats:title>ABSTRACT</jats:title><jats:p>Infection of humans with<jats:italic>Ehrlichia chaffeensis</jats:italic>, the etiologic agent of human monocytic ehrlichiosis, can cause hepatitis of various levels of severity. When the three human isolates of<jats:italic>E. chaffeensis</jats:italic>, each belonging to a different genogroup, are inoculated into severe combined immunodeficiency mice, the order of severity of clinical signs and bacterial burden detected in the liver is as follows (from greatest to least severity and highest to lowest burden): strain Wakulla, followed by strain Liberty, followed by strain Arkansas. In this article, we used microarray analysis to define transcriptional profiles characteristic of the histopathological features in the mouse liver. Cytokine and chemokine profiles and their receptor profiles were strikingly different among the three strains of<jats:italic>E. chaffeensis</jats:italic>: gamma interferon, CCL5, CXCL1, CXCL2, CXCL7, CXCL9, interleukin 2 receptor gamma (IL2Rγ), IL21R, CCR2, and CXCR6 were highly upregulated with strain Arkansas; and tumor necrosis factor (TNF), CCL2, CCL3, CCL5, CCL6, CCL12, CCL20, CXCL2, CXCL7, CXCL9, CXCL13, TNF receptor superfamily 9 (TNFRSF9), TNFRSF13β, IL1R2, IL2Rγ, IL20Rβ, IL21R, CCR1, CCR2, and CXCR4 were highly upregulated with strain Wakulla. With strain Liberty, only CXCL13 was highly upregulated, and IL13Rα2 was downregulated. In livers infected with the Arkansas strain, monocytes/macrophages and NK cells were enriched in the granulomas and an increase in NK cell marker mRNAs was detected. Livers infected with the Wakulla strain displayed infiltration of significantly more neutrophils and an increase in neutrophil marker mRNAs. Genes commonly upregulated in liver tissue infected with the three strains are other host innate immune and inflammatory response genes, including those encoding several acute-phase proteins. Genes downregulated commonly are related to host physiologic functions. The results suggest that marked modulation of host cytokine and chemokine profiles by<jats:italic>E. chaffeensis</jats:italic>strains underlies the distinct host liver disease.</jats:p>
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author Miura, Koshiro, Rikihisa, Yasuko
author_facet Miura, Koshiro, Rikihisa, Yasuko, Miura, Koshiro, Rikihisa, Yasuko
author_sort miura, koshiro
container_issue 1
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container_title Infection and Immunity
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description <jats:title>ABSTRACT</jats:title><jats:p>Infection of humans with<jats:italic>Ehrlichia chaffeensis</jats:italic>, the etiologic agent of human monocytic ehrlichiosis, can cause hepatitis of various levels of severity. When the three human isolates of<jats:italic>E. chaffeensis</jats:italic>, each belonging to a different genogroup, are inoculated into severe combined immunodeficiency mice, the order of severity of clinical signs and bacterial burden detected in the liver is as follows (from greatest to least severity and highest to lowest burden): strain Wakulla, followed by strain Liberty, followed by strain Arkansas. In this article, we used microarray analysis to define transcriptional profiles characteristic of the histopathological features in the mouse liver. Cytokine and chemokine profiles and their receptor profiles were strikingly different among the three strains of<jats:italic>E. chaffeensis</jats:italic>: gamma interferon, CCL5, CXCL1, CXCL2, CXCL7, CXCL9, interleukin 2 receptor gamma (IL2Rγ), IL21R, CCR2, and CXCR6 were highly upregulated with strain Arkansas; and tumor necrosis factor (TNF), CCL2, CCL3, CCL5, CCL6, CCL12, CCL20, CXCL2, CXCL7, CXCL9, CXCL13, TNF receptor superfamily 9 (TNFRSF9), TNFRSF13β, IL1R2, IL2Rγ, IL20Rβ, IL21R, CCR1, CCR2, and CXCR4 were highly upregulated with strain Wakulla. With strain Liberty, only CXCL13 was highly upregulated, and IL13Rα2 was downregulated. In livers infected with the Arkansas strain, monocytes/macrophages and NK cells were enriched in the granulomas and an increase in NK cell marker mRNAs was detected. Livers infected with the Wakulla strain displayed infiltration of significantly more neutrophils and an increase in neutrophil marker mRNAs. Genes commonly upregulated in liver tissue infected with the three strains are other host innate immune and inflammatory response genes, including those encoding several acute-phase proteins. Genes downregulated commonly are related to host physiologic functions. The results suggest that marked modulation of host cytokine and chemokine profiles by<jats:italic>E. chaffeensis</jats:italic>strains underlies the distinct host liver disease.</jats:p>
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spelling Miura, Koshiro Rikihisa, Yasuko 0019-9567 1098-5522 American Society for Microbiology Infectious Diseases Immunology Microbiology Parasitology http://dx.doi.org/10.1128/iai.00979-08 <jats:title>ABSTRACT</jats:title><jats:p>Infection of humans with<jats:italic>Ehrlichia chaffeensis</jats:italic>, the etiologic agent of human monocytic ehrlichiosis, can cause hepatitis of various levels of severity. When the three human isolates of<jats:italic>E. chaffeensis</jats:italic>, each belonging to a different genogroup, are inoculated into severe combined immunodeficiency mice, the order of severity of clinical signs and bacterial burden detected in the liver is as follows (from greatest to least severity and highest to lowest burden): strain Wakulla, followed by strain Liberty, followed by strain Arkansas. In this article, we used microarray analysis to define transcriptional profiles characteristic of the histopathological features in the mouse liver. Cytokine and chemokine profiles and their receptor profiles were strikingly different among the three strains of<jats:italic>E. chaffeensis</jats:italic>: gamma interferon, CCL5, CXCL1, CXCL2, CXCL7, CXCL9, interleukin 2 receptor gamma (IL2Rγ), IL21R, CCR2, and CXCR6 were highly upregulated with strain Arkansas; and tumor necrosis factor (TNF), CCL2, CCL3, CCL5, CCL6, CCL12, CCL20, CXCL2, CXCL7, CXCL9, CXCL13, TNF receptor superfamily 9 (TNFRSF9), TNFRSF13β, IL1R2, IL2Rγ, IL20Rβ, IL21R, CCR1, CCR2, and CXCR4 were highly upregulated with strain Wakulla. With strain Liberty, only CXCL13 was highly upregulated, and IL13Rα2 was downregulated. In livers infected with the Arkansas strain, monocytes/macrophages and NK cells were enriched in the granulomas and an increase in NK cell marker mRNAs was detected. Livers infected with the Wakulla strain displayed infiltration of significantly more neutrophils and an increase in neutrophil marker mRNAs. Genes commonly upregulated in liver tissue infected with the three strains are other host innate immune and inflammatory response genes, including those encoding several acute-phase proteins. Genes downregulated commonly are related to host physiologic functions. The results suggest that marked modulation of host cytokine and chemokine profiles by<jats:italic>E. chaffeensis</jats:italic>strains underlies the distinct host liver disease.</jats:p> Liver Transcriptome Profiles Associated with Strain-Specific<i>Ehrlichia chaffeensis</i>-Induced Hepatitis in SCID Mice Infection and Immunity
spellingShingle Miura, Koshiro, Rikihisa, Yasuko, Infection and Immunity, Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice, Infectious Diseases, Immunology, Microbiology, Parasitology
title Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_full Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_fullStr Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_full_unstemmed Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_short Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
title_sort liver transcriptome profiles associated with strain-specific<i>ehrlichia chaffeensis</i>-induced hepatitis in scid mice
title_unstemmed Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice
topic Infectious Diseases, Immunology, Microbiology, Parasitology
url http://dx.doi.org/10.1128/iai.00979-08