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  1. Article: Modulation of host cell death pathways by Yersinia species and the type III effector YopK.

    Peters, Kristen N / Anderson, Deborah M

    Advances in experimental medicine and biology

    2012  Volume 954, Page(s) 229–236

    MeSH term(s) Animals ; Bacterial Outer Membrane Proteins/physiology ; Bacterial Proteins/physiology ; Cells, Cultured ; Cysteine Endopeptidases/physiology ; Female ; Mice ; Mice, Inbred BALB C ; Yersinia/pathogenicity
    Chemical Substances Bacterial Outer Membrane Proteins ; Bacterial Proteins ; YopP protein, Yersinia ; YopT protein, Yersinia ; yopE protein, Yersinia ; Cysteine Endopeptidases (EC 3.4.22.-)
    Language English
    Publishing date 2012
    Publishing country United States
    Document type Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-1-4614-3561-7_29
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Zika virus induced cellular remodelling.

    Rossignol, Evan D / Peters, Kristen N / Connor, John H / Bullitt, Esther

    Cellular microbiology

    2017  Volume 19, Issue 8

    Abstract: Zika virus (ZIKV) has been associated with morbidities such as Guillain-Barré, infant microcephaly, and ocular disease. The spread of this positive-sense, single-stranded RNA virus and its growing public health threat underscore gaps in our understanding ...

    Abstract Zika virus (ZIKV) has been associated with morbidities such as Guillain-Barré, infant microcephaly, and ocular disease. The spread of this positive-sense, single-stranded RNA virus and its growing public health threat underscore gaps in our understanding of basic ZIKV virology. To advance knowledge of the virus replication cycle within mammalian cells, we use serial section 3-dimensional electron tomography to demonstrate the widespread remodelling of intracellular membranes upon infection with ZIKV. We report extensive structural rearrangements of the endoplasmic reticulum and reveal stages of the ZIKV viral replication cycle. Structures associated with RNA genome replication and virus assembly are observed integrated within the endoplasmic reticulum, and we show viruses in transit through the Golgi apparatus for viral maturation, and subsequent cellular egress. This study characterises in detail the 3-dimensional ultrastructural organisation of the ZIKV replication cycle stages. Our results show close adherence of the ZIKV replication cycle to the existing flavivirus replication paradigm.
    MeSH term(s) Animals ; Cercopithecus aethiops ; Electron Microscope Tomography ; Endoplasmic Reticulum/ultrastructure ; Endoplasmic Reticulum/virology ; Golgi Apparatus/ultrastructure ; Golgi Apparatus/virology ; Host-Pathogen Interactions ; Imaging, Three-Dimensional ; Vero Cells ; Virus Assembly ; Virus Release ; Virus Replication ; Zika Virus/physiology ; Zika Virus/ultrastructure
    Language English
    Publishing date 2017
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1468320-9
    ISSN 1462-5822 ; 1462-5814
    ISSN (online) 1462-5822
    ISSN 1462-5814
    DOI 10.1111/cmi.12740
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  3. Article ; Online: Macrophages clean up: efferocytosis and microbial control.

    Martin, Constance J / Peters, Kristen N / Behar, Samuel M

    Current opinion in microbiology

    2013  Volume 17, Page(s) 17–23

    Abstract: Phagocytic leukocytes, predominantly macrophages, not only ingest and destroy invading pathogens, but are charged with clearing dead and dying host cells. The process of engulfing apoptotic cells is called efferocytosis and has long been appreciated for ... ...

    Abstract Phagocytic leukocytes, predominantly macrophages, not only ingest and destroy invading pathogens, but are charged with clearing dead and dying host cells. The process of engulfing apoptotic cells is called efferocytosis and has long been appreciated for its role in the resolution of inflammation. New evidence is emerging that efferocytosis represents a double-edged sword in microbial immunity. Although efferocytosis of influenza and Mycobacterium tuberculosis-infected cells results in pathogen destruction, efferocytosis of Leishmania-infected neutrophils may promote infection. Understanding how macrophages, dendritic cells (DC) and neutrophils process pathogens encased within a dying cell could lead to the development of novel therapeutics that simultaneously suppress inflammation and promote pathogen clearance.
    MeSH term(s) Animals ; Bacteria ; Dendritic Cells ; Host-Pathogen Interactions ; Humans ; Leishmania ; Macrophages ; Mice ; Models, Immunological ; Neutrophils ; Phagocytosis
    Language English
    Publishing date 2013-12-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1418474-6
    ISSN 1879-0364 ; 1369-5274
    ISSN (online) 1879-0364
    ISSN 1369-5274
    DOI 10.1016/j.mib.2013.10.007
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  4. Article: Macrophages clean up: efferocytosis and microbial control

    Martin, Constance J / Peters, Kristen N / Behar, Samuel M

    Current opinion in microbiology. 2014 Feb., v. 17

    2014  

    Abstract: Phagocytic leukocytes, predominantly macrophages, not only ingest and destroy invading pathogens, but are charged with clearing dead and dying host cells. The process of engulfing apoptotic cells is called efferocytosis and has long been appreciated for ... ...

    Abstract Phagocytic leukocytes, predominantly macrophages, not only ingest and destroy invading pathogens, but are charged with clearing dead and dying host cells. The process of engulfing apoptotic cells is called efferocytosis and has long been appreciated for its role in the resolution of inflammation. New evidence is emerging that efferocytosis represents a double-edged sword in microbial immunity. Although efferocytosis of influenza and Mycobacterium tuberculosis-infected cells results in pathogen destruction, efferocytosis of Leishmania-infected neutrophils may promote infection. Understanding how macrophages, dendritic cells (DC) and neutrophils process pathogens encased within a dying cell could lead to the development of novel therapeutics that simultaneously suppress inflammation and promote pathogen clearance.
    Keywords Mycobacterium tuberculosis ; apoptosis ; dendritic cells ; immunity ; inflammation ; influenza ; macrophages ; neutrophils ; pathogens ; therapeutics
    Language English
    Dates of publication 2014-02
    Size p. 17-23.
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 1418474-6
    ISSN 1879-0364 ; 1369-5274
    ISSN (online) 1879-0364
    ISSN 1369-5274
    DOI 10.1016/j.mib.2013.10.007
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  5. Article ; Online: Early apoptosis of macrophages modulated by injection of Yersinia pestis YopK promotes progression of primary pneumonic plague.

    Peters, Kristen N / Dhariwala, Miqdad O / Hughes Hanks, Jennifer M / Brown, Charles R / Anderson, Deborah M

    PLoS pathogens

    2013  Volume 9, Issue 4, Page(s) e1003324

    Abstract: Yersinia pestis causes pneumonic plague, a disease characterized by inflammation, necrosis and rapid bacterial growth which together cause acute lung congestion and lethality. The bacterial type III secretion system (T3SS) injects 7 effector proteins ... ...

    Abstract Yersinia pestis causes pneumonic plague, a disease characterized by inflammation, necrosis and rapid bacterial growth which together cause acute lung congestion and lethality. The bacterial type III secretion system (T3SS) injects 7 effector proteins into host cells and their combined activities are necessary to establish infection. Y. pestis infection of the lungs proceeds as a biphasic inflammatory response believed to be regulated through the control of apoptosis and pyroptosis by a single, well-conserved T3SS effector protein YopJ. Recently, YopJ-mediated pyroptosis, which proceeds via the NLRP3-inflammasome, was shown to be regulated by a second T3SS effector protein YopK in the related strain Y. pseudotuberculosis. In this work, we show that for Y. pestis, YopK appears to regulate YopJ-mediated apoptosis, rather than pyroptosis, of macrophages. Inhibition of caspase-8 blocked YopK-dependent apoptosis, suggesting the involvement of the extrinsic pathway, and appeared cell-type specific. However, in contrast to yopJ, deletion of yopK caused a large decrease in virulence in a mouse pneumonic plague model. YopK-dependent modulation of macrophage apoptosis was observed at 6 and 24 hours post-infection (HPI). When YopK was absent, decreased populations of macrophages and dendritic cells were seen in the lungs at 24 HPI and correlated with resolution rather than progression of inflammation. Together the data suggest that Y. pestis YopK may coordinate the inflammatory response during pneumonic plague through the regulation of apoptosis of immune cells.
    MeSH term(s) Animals ; Apoptosis ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Bacterial Secretion Systems ; Caspase 3/metabolism ; Caspase 8/metabolism ; Dendritic Cells/metabolism ; Enzyme Activation ; Female ; Macrophages/immunology ; Macrophages/physiology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Plague/immunology ; Promoter Regions, Genetic ; Yersinia pestis/immunology ; Yersinia pestis/metabolism ; Yersinia pestis/pathogenicity
    Chemical Substances Apoptosis Regulatory Proteins ; Bacterial Proteins ; Bacterial Secretion Systems ; YopP protein, Yersinia ; Caspase 3 (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2013-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1003324
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  6. Article ; Online: Remote monitoring of the progression of primary pneumonic plague in Brown Norway rats in high-capacity, high-containment housing.

    Coate, Eric A / Kocsis, Andrew G / Peters, Kristen N / Anderson, Paul E / Ellersieck, Mark R / Fine, Deborah M / Anderson, Deborah M

    Pathogens and disease

    2014  Volume 71, Issue 2, Page(s) 265–275

    Abstract: Development of new vaccines, diagnostics, and therapeutics for biodefense or other relatively rare infectious diseases is hindered by the lack of naturally occurring human disease on which to conduct clinical trials of efficacy. To overcome this ... ...

    Abstract Development of new vaccines, diagnostics, and therapeutics for biodefense or other relatively rare infectious diseases is hindered by the lack of naturally occurring human disease on which to conduct clinical trials of efficacy. To overcome this experimental gap, the U.S. Food and Drug Administration established the Animal Rule, in which efficacy testing in two well-characterized animal models that closely resemble human disease may be accepted in lieu of large-scale clinical trials for diseases with limited natural human incidence. In this report, we evaluated the Brown Norway rat as a model for pneumonic plague and describe the natural history of clinical disease following inhalation exposure to Yersinia pestis. In high-capacity, high-containment housing, we monitored temperature, activity, heart rate, and rhythm by capturing electronic impulses transmitted from abdominal telemeter implants. Using this system, we show that reduced activity and development of fever are sensitive indications of disease progression. Furthermore, we identified heart arrhythmias as contributing factors to the rapid progression to lethality following the fever response. Together, these data validate the Brown Norway rat as an experimental model for human pneumonic plague and provide new insight that may ultimately lead to novel approaches in postexposure treatment of this devastating infection.
    MeSH term(s) Animals ; Body Temperature ; Containment of Biohazards/methods ; Disease Models, Animal ; Female ; Heart Rate ; Inhalation Exposure ; Male ; Motor Activity ; Plague/pathology ; Rats ; Remote Sensing Technology/methods ; Yersinia pestis/pathogenicity
    Language English
    Publishing date 2014-05-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2049-632X
    ISSN (online) 2049-632X
    DOI 10.1111/2049-632X.12176
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  7. Article ; Online: Host stress and immune responses during aerosol challenge of Brown Norway rats with Yersinia pestis.

    Gater, Susan T / Peters, Kristen N / Kocsis, Andrew G / Dhariwala, Miqdad O / Anderson, Deborah M / Anderson, Paul E

    Frontiers in cellular and infection microbiology

    2012  Volume 2, Page(s) 147

    Abstract: Inhalation exposure models are becoming the preferred method for the comparative study of respiratory infectious diseases due to their resemblance to the natural route of infection. To enable precise delivery of pathogen to the lower respiratory tract in ...

    Abstract Inhalation exposure models are becoming the preferred method for the comparative study of respiratory infectious diseases due to their resemblance to the natural route of infection. To enable precise delivery of pathogen to the lower respiratory tract in a manner that imposes minimal biosafety risk, nose-only exposure systems have been developed. Early inhalation exposure technology for infectious disease research grew out of technology used in asthma research where predominantly the Collison nebulizer is used to generate an aerosol by beating a liquid sample against glass. Although infectious aerosol droplets of 1-5 μm in size can be generated, the Collison often causes loss of viability. In this work, we evaluate a gentler method for aerosolization of living cells and describe the use of the Sparging Liquid Aerosol Generator (SLAG) in a rat pneumonic plague model. The SLAG creates aerosols by continuous dripping of liquid sample on a porous metal disc. We show the generation of 0.5-1 μm Yersinia pestis aerosol particles using the SLAG with spray factors typically ranging from 10(-7) to 10(-8) with no detectable loss of bacterial viability. Delivery of these infectious particles via nose-only exposure led to the rapid development of lethal pneumonic plague. Further, we evaluated the effect of restraint-stress imposed by the nose-only exposure chamber on early inflammatory responses and bacterial deposition. Elevated serum corticosterone which peaked at 2 h post-procedure indicated the animals experienced stress as a result of restraint in the nose-only chamber. However, we observed no correlation between elevated corticosterone and the amount of bacterial deposition or inflammation in the lungs. Together these data demonstrate the utility of the SLAG and the nose-only chamber for aerosol challenge of rodents by Y. pestis.
    MeSH term(s) Aerosols ; Animals ; Corticosterone/blood ; Disease Models, Animal ; Female ; Inhalation Exposure ; Male ; Nasal Sprays ; Nebulizers and Vaporizers/microbiology ; Plague/pathology ; Rats ; Stress, Psychological/diagnosis ; Time Factors ; Yersinia pestis/pathogenicity
    Chemical Substances Aerosols ; Nasal Sprays ; Corticosterone (W980KJ009P)
    Language English
    Publishing date 2012-11-30
    Publishing country Switzerland
    Document type Evaluation Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2012.00147
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  8. Article ; Online: PERP, a host tetraspanning membrane protein, is required for Salmonella-induced inflammation.

    Hallstrom, Kelly N / Srikanth, C V / Agbor, Terence A / Dumont, Christopher M / Peters, Kristen N / Paraoan, Luminita / Casanova, James E / Boll, Erik J / McCormick, Beth A

    Cellular microbiology

    2015  Volume 17, Issue 6, Page(s) 843–859

    Abstract: Salmonella enterica Typhimurium induces intestinal inflammation through the activity of type III secreted effector (T3SE) proteins. Our prior results indicate that the secretion of the T3SE SipA and the ability of SipA to induce epithelial cell responses ...

    Abstract Salmonella enterica Typhimurium induces intestinal inflammation through the activity of type III secreted effector (T3SE) proteins. Our prior results indicate that the secretion of the T3SE SipA and the ability of SipA to induce epithelial cell responses that lead to induction of polymorphonuclear transepithelial migration are not coupled to its direct delivery into epithelial cells from Salmonella. We therefore tested the hypothesis that SipA interacts with a membrane protein located at the apical surface of intestinal epithelial cells. Employing a split ubiquitin yeast-two-hybrid screen, we identified the tetraspanning membrane protein, p53 effector related to PMP-22 (PERP), as a SipA binding partner. SipA and PERP appear to have intersecting activities as we found PERP to be involved in proinflammatory pathways shown to be regulated by SipA. In sum, our studies reveal a critical role for PERP in the pathogenesis of S. Typhimurium, and for the first time demonstrate that SipA, a T3SE protein, can engage a host protein at the epithelial surface.
    MeSH term(s) Bacterial Proteins/metabolism ; Cell Line ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Genes, Tumor Suppressor ; Host-Pathogen Interactions ; Humans ; Inflammation/microbiology ; Inflammation/pathology ; Membrane Proteins/metabolism ; Microfilament Proteins/metabolism ; Protein Binding ; Protein Interaction Mapping ; Salmonella typhimurium/immunology ; Transendothelial and Transepithelial Migration ; Two-Hybrid System Techniques
    Chemical Substances Bacterial Proteins ; Membrane Proteins ; Microfilament Proteins ; PERP protein, human ; SipA protein, Salmonella
    Language English
    Publishing date 2015-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 1468320-9
    ISSN 1462-5822 ; 1462-5814
    ISSN (online) 1462-5822
    ISSN 1462-5814
    DOI 10.1111/cmi.12406
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