Caspase-1 Mediates Resistance in Murine Melioidosis

The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell...

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Published inInfection and Immunity Vol. 77; no. 4; pp. 1589 - 1595
Main Authors Breitbach, Katrin, Sun, Guang Wen, Köhler, Jens, Eske, Kristin, Wongprompitak, Patimaporn, Tan, Gladys, Liu, Yichun, Gan, Yunn-Hwen, Steinmetz, Ivo
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.04.2009
American Society for Microbiology (ASM)
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Abstract The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that B. pseudomallei can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during B. pseudomallei infection. In vivo experiments with caspase-1⁻/⁻ mice revealed a high susceptibility to B. pseudomallei challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-γ) and interleukin-18 cytokine levels 24 h after infection compared to control animals. caspase-1⁻/⁻ bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early B. pseudomallei infection, indicating "classical" apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that caspase-1⁻/⁻ BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for B. pseudomallei, but, in addition, caspase-1 might also have a role in controlling intracellular replication of B. pseudomallei in macrophages. Moreover, caspase-1-dependent IFN-γ production is likely to contribute to resistance in murine melioidosis.
AbstractList The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that B. pseudomallei can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during B. pseudomallei infection. In vivo experiments with caspase-1-/- mice revealed a high susceptibility to B. pseudomallei challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-) and interleukin-18 cytokine levels 24 h after infection compared to control animals. caspase-1-/- bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early B. pseudomallei infection, indicating QUOTATION_MARKclassicalQUOTATION_MARK apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that caspase-1-/- BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for B. pseudomallei, but, in addition, caspase-1 might also have a role in controlling intracellular replication of B. pseudomallei in macrophages. Moreover, caspase-1-dependent IFN- production is likely to contribute to resistance in murine melioidosis.
The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that B. pseudomallei can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during B. pseudomallei infection. In vivo experiments with caspase-1⁻/⁻ mice revealed a high susceptibility to B. pseudomallei challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-γ) and interleukin-18 cytokine levels 24 h after infection compared to control animals. caspase-1⁻/⁻ bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early B. pseudomallei infection, indicating "classical" apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that caspase-1⁻/⁻ BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for B. pseudomallei, but, in addition, caspase-1 might also have a role in controlling intracellular replication of B. pseudomallei in macrophages. Moreover, caspase-1-dependent IFN-γ production is likely to contribute to resistance in murine melioidosis.
The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that B. pseudomallei can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during B. pseudomallei infection. In vivo experiments with caspase-1 −/− mice revealed a high susceptibility to B. pseudomallei challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-γ) and interleukin-18 cytokine levels 24 h after infection compared to control animals. caspase-1 −/− bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early B. pseudomallei infection, indicating “classical” apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that caspase-1 −/− BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for B. pseudomallei , but, in addition, caspase-1 might also have a role in controlling intracellular replication of B. pseudomallei in macrophages. Moreover, caspase-1-dependent IFN-γ production is likely to contribute to resistance in murine melioidosis.
The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical areas. The bacterium multiplies intracellularly within the cytosol, induces the formation of actin tails, and can spread directly from cell to cell. Recently, it has been shown that B. pseudomallei can induce caspase-1-dependent cell death in macrophages. The aim of the present study was to further elucidate the role of caspase-1 during B. pseudomallei infection. In vivo experiments with caspase-1(-/-) mice revealed a high susceptibility to B. pseudomallei challenge. This phenotype was associated with a significantly higher bacterial burden 2 days after infection and decreased gamma interferon (IFN-gamma) and interleukin-18 cytokine levels 24 h after infection compared to control animals. caspase-1(-/-) bone marrow-derived macrophages (BMM) exhibited strong caspase-3 expression and reduced cell damage compared to wild-type (WT) cells during early B. pseudomallei infection, indicating "classical" apoptosis, whereas WT BMM showed signs of rapid caspase-1-dependent cell death. Moreover, we found that caspase-1(-/-) BMM had a strongly increased bacterial burden compared to WT cells 3 h after infection under conditions where no difference in cell death could be observed between both cell populations at this time point. We therefore suggest that caspase-1-dependent rapid cell death might contribute to resistance by reducing the intracellular niche for B. pseudomallei, but, in addition, caspase-1 might also have a role in controlling intracellular replication of B. pseudomallei in macrophages. Moreover, caspase-1-dependent IFN-gamma production is likely to contribute to resistance in murine melioidosis.
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Author Sun, Guang Wen
Liu, Yichun
Steinmetz, Ivo
Breitbach, Katrin
Köhler, Jens
Eske, Kristin
Gan, Yunn-Hwen
Wongprompitak, Patimaporn
Tan, Gladys
AuthorAffiliation Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany, 1 Department of Biochemistry, National University of Singapore, Singapore, Republic of Singapore, 2 Department of Immunology, Faculty of Medicine Siriraj, Mahidol University, Bangkok, Thailand, 3 Defence Medical and Environmental Research Institute, DSO National Laboratories, Singapore, Republic of Singapore 4
AuthorAffiliation_xml – name: Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany, 1 Department of Biochemistry, National University of Singapore, Singapore, Republic of Singapore, 2 Department of Immunology, Faculty of Medicine Siriraj, Mahidol University, Bangkok, Thailand, 3 Defence Medical and Environmental Research Institute, DSO National Laboratories, Singapore, Republic of Singapore 4
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Issue 4
Keywords Microbiology
Enzyme
Rodentia
Caspase
Immunity
Infection
Melioidosis
Resistance
Peptidases
Vertebrata
Mammalia
Mouse
Bacteriosis
Hydrolases
Language English
License CC BY 4.0
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Editor: S. R. Blanke
Corresponding author. Mailing address: Friedrich Loeffler Institute of Medical Microbiology, Ernst Moritz Arndt University Greifswald, Martin Luther Str. 6, 17489 Greifswald, Germany. Phone: 49 (0) 3834 865587. Fax: 49 (0) 3834 865561. E-mail: steinmetz.ivo@uni-greifswald.de
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Snippet The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical...
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The gram-negative rod Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease which is endemic in tropical and subtropical...
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SourceType Open Access Repository
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SubjectTerms Actin
Animals
Apoptosis
Bacterial diseases
Bacterial Infections
Biological and medical sciences
Bone marrow
Bone Marrow Cells - cytology
Burkholderia pseudomallei
Burkholderia pseudomallei - growth & development
Burkholderia pseudomallei - pathogenicity
Burkholderia pseudomallei - physiology
Caspase 1 - metabolism
Caspase-1
Caspase-3
Cytosol
Down-Regulation
Female
Fundamental and applied biological sciences. Psychology
g-Interferon
Human bacterial diseases
Humans
Infection
Infectious diseases
Interferon
Interferon-gamma - metabolism
Interleukin 18
Interleukin-18 - metabolism
Lymphocytes B
Macrophages
Macrophages - cytology
Macrophages - microbiology
Male
Medical sciences
Melioidosis
Melioidosis - immunology
Melioidosis - microbiology
Melioidosis - mortality
Mice
Mice, Inbred C57BL
Microbiology
Replication
Tails
Tropical bacterial diseases
Title Caspase-1 Mediates Resistance in Murine Melioidosis
URI http://iai.asm.org/content/77/4/1589.abstract
https://www.ncbi.nlm.nih.gov/pubmed/19179418
https://search.proquest.com/docview/21477740
https://search.proquest.com/docview/67030894
https://pubmed.ncbi.nlm.nih.gov/PMC2663179
Volume 77
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