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  1. Article ; Online: Evaluation of surrogate animal models of melioidosis.

    Warawa, Jonathan Mark

    Frontiers in microbiology

    2010  Volume 1, Page(s) 141

    Abstract: Burkholderia pseudomallei is the Gram-negative bacterial pathogen responsible for the disease melioidosis. B. pseudomallei establishes disease in susceptible individuals through multiple routes of infection, all of which may proceed to a septicemic ... ...

    Abstract Burkholderia pseudomallei is the Gram-negative bacterial pathogen responsible for the disease melioidosis. B. pseudomallei establishes disease in susceptible individuals through multiple routes of infection, all of which may proceed to a septicemic disease associated with a high mortality rate. B. pseudomallei opportunistically infects humans and a wide range of animals directly from the environment, and modeling of experimental melioidosis has been conducted in numerous biologically relevant models including mammalian and invertebrate hosts. This review seeks to summarize published findings related to established animal models of melioidosis, with an aim to compare and contrast the virulence of B. pseudomallei in these models. The effect of the route of delivery on disease is also discussed for intravenous, intraperitoneal, subcutaneous, intranasal, aerosol, oral, and intratracheal infection methodologies, with a particular focus on how they relate to modeling clinical melioidosis. The importance of the translational validity of the animal models used in B. pseudomallei research is highlighted as these studies have become increasingly therapeutic in nature.
    Language English
    Publishing date 2010-12-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587354-4
    ISSN 1664-302X ; 1664-302X
    ISSN (online) 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2010.00141
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Recombinant Human Plasma Gelsolin Improves Survival and Attenuates Lung Injury in a Murine Model of Multidrug-Resistant

    DiNubile, Mark J / Levinson, Susan L / Stossel, Thomas P / Lawrenz, Matthew B / Warawa, Jonathan M

    Open forum infectious diseases

    2020  Volume 7, Issue 8, Page(s) ofaa236

    Abstract: ... by extensive tissue damage. Marked depletion is associated with later poor outcomes in diverse clinical ...

    Abstract Background: Plasma gelsolin (pGSN) is an abundant circulating protein quickly consumed by extensive tissue damage. Marked depletion is associated with later poor outcomes in diverse clinical circumstances. Repletion with recombinant human (rhu)-pGSN in animal models of inflammation lessens mortality and morbidity.
    Methods: Neutropenic mice were treated with different meropenem doses ±12 mg of rhu-pGSN commencing 1 day before an intratracheal challenge with multidrug-resistant
    Results: Overall survival was 35/64 (55%) and 46/64 (72%) in mice given meropenem without and with rhu-pGSN, respectively (Δ = 17%; 95% CI, 1-34). In control mice receiving meropenem 1250 mg/kg/d where the majority died, the addition of rhu-pGSN increased survival from 5/16 (31%) to 12/16 (75%) (Δ = 44%; 95% CI, 13-75). Survival with minor lung injury was found in 26/64 (41%) mice receiving only meropenem, vs 38/64 (59%) in mice given meropenem plus rhu-pGSN (Δ = 19%; 95% CI, 2-36).
    Conclusions: In a series of dose-ranging experiments, both mortality and lung injury were reduced by the addition of rhu-pGSN to meropenem against carbapenem-resistant
    Language English
    Publishing date 2020-06-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2757767-3
    ISSN 2328-8957
    ISSN 2328-8957
    DOI 10.1093/ofid/ofaa236
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Co-ordinate regulation of distinct host cell signalling pathways by multifunctional enteropathogenic Escherichia coli effector molecules.

    Kenny, Brendan / Ellis, Sarah / Leard, Alan D / Warawa, Jonathan / Mellor, Harry / Jepson, Mark A

    Molecular microbiology

    2002  Volume 44, Issue 4, Page(s) 1095–1107

    Abstract: Enteropathogenic Escherichia coli (EPEC) is a major cause of paediatric diarrhoea and a model for the family of attaching and effacing (A/E) pathogens. A/E pathogens encode a type III secretion system to transfer effector proteins into host cells. The ... ...

    Abstract Enteropathogenic Escherichia coli (EPEC) is a major cause of paediatric diarrhoea and a model for the family of attaching and effacing (A/E) pathogens. A/E pathogens encode a type III secretion system to transfer effector proteins into host cells. The EPEC Tir effector protein acts as a receptor for the bacterial surface protein intimin and is involved in the formation of Cdc42-independent, actin-rich pedestal structures beneath the adhered bacteria. In this paper, we demonstrate that EPEC binding to HeLa cells also induces Tir-independent, cytoskeletal rearrangement evidenced by the early, transient formation of filopodia-like structures at sites of infection. Filopodia formation is dependent on expression of the EPEC Map effector molecule - a protein that targets mitochondria and induces their dysfunction. We show that Map-induced filopodia formation is independent of mitochondrial targeting and is abolished by cellular expression of the Cdc42 inhibitory WASP-CRIB domain, demonstrating that Map has at least two distinct functions in host cells. The transient nature of the filopodia is related to an ability of EPEC to downregulate Map-induced cell signalling that, like pedestal formation, was dependent on both Tir and intimin proteins. The ability of Tir to downregulate filopodia was impaired by disrupting a putative GTPase-activating protein (GAP) motif, suggesting that Tir may possess such a function, with its interaction with intimin triggering this activity. Furthermore, we also found that Map-induced cell signalling inhibits pedestal formation, revealing that the cellular effects of Tir and Map must be co-ordinately regulated during infection. Possible implications of the multifunctional nature of EPEC effector molecules in pathogenesis are discussed.
    MeSH term(s) Actins/metabolism ; Adhesins, Bacterial/metabolism ; Bacterial Adhesion ; Carrier Proteins/metabolism ; Cytoskeleton/metabolism ; Cytoskeleton/microbiology ; Diarrhea/metabolism ; Diarrhea/microbiology ; Down-Regulation ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Escherichia coli/pathogenicity ; Escherichia coli/ultrastructure ; Escherichia coli Infections/metabolism ; Escherichia coli Infections/microbiology ; Escherichia coli Proteins ; HeLa Cells ; Humans ; Models, Biological ; Protein Binding ; Pseudopodia/physiology ; Receptors, Cell Surface/metabolism ; Signal Transduction ; cdc42 GTP-Binding Protein/metabolism
    Chemical Substances Actins ; Adhesins, Bacterial ; Carrier Proteins ; Escherichia coli Proteins ; Receptors, Cell Surface ; Tir protein, E coli ; eaeA protein, E coli (147094-99-3) ; cdc42 GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2002-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 619315-8
    ISSN 1365-2958 ; 0950-382X
    ISSN (online) 1365-2958
    ISSN 0950-382X
    DOI 10.1046/j.1365-2958.2002.02952.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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