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  • 1
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    An immunoaffinity tandem mass spectrometry (iMALDI) assay for detection of Francisella tularensis
    Elsevier BV ; 2007
    In:  Analytica Chimica Acta Vol. 605, No. 1 ( 2007-12), p. 70-79
    Details
    In: Analytica Chimica Acta, Elsevier BV, Vol. 605, No. 1 ( 2007-12), p. 70-79
    Type of Medium: Online Resource
    ISSN: 0003-2670
    URL: Article
    DOI: 10.1016/j.aca.2007.10.025
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 52-8
    detail.hit.zdb_id: 1483436-4
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  • 2
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    A Superoxide Dismutase C Mutant of Haemophilus ducreyi Is Virulent in Human Volunteers
    American Society for Microbiology ; 2002
    In:  Infection and Immunity Vol. 70, No. 3 ( 2002-03), p. 1367-1371
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 70, No. 3 ( 2002-03), p. 1367-1371
    Abstract: Haemophilus ducreyi produces a periplasmic copper-zinc superoxide dismutase (Cu-Zn SOD), which is thought to protect the organism from exogenous reactive oxygen species generated by neutrophils during an inflammatory response. We had previously identified the gene, sodC , responsible for the production and secretion of Cu-Zn SOD and constructed an isogenic H. ducreyi strain with a mutation in the sodC gene (35000HP- sodC-cat ). Compared to the parent, the mutant does not survive in the presence of exogenous superoxide (L. R. San Mateo, M. Hobbs, and T. H. Kawula, Mol. Microbiol. 27:391-404, 1998) and is impaired in the swine model of H. ducreyi infection (L. R. San Mateo, K. L. Toffer, P. E. Orndorff, and T. H. Kawula, Infect. Immun. 67:5345-5351, 1999). To test whether Cu-Zn SOD is important for bacterial survival in vivo, six human volunteers were experimentally infected with 35000HP and 35000HP- sodC-cat and observed for papule and pustule formation. Papules developed at similar rates at sites inoculated with the mutant or parent. The pustule formation rates were 75% (95% confidence intervals [CI], 43 to 95%) at 12 parent-inoculated sites and 67% (95% CI, 41 to 88%) at 18 mutant-inoculated sites ( P = 0.47). There was no significant difference in levels of H. ducreyi recovery from mutant- and parent-inoculated biopsy sites. These results suggest that expression of Cu-Zn SOD does not play a major role in the survival of this pathogen in the initial stages of experimental infection of humans.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.70.3.1367-1371.2002
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2002
    detail.hit.zdb_id: 1483247-1
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  • 3
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    Effects of the Putative Transcriptional Regulator IclR on Francisella tularensis Pathogenesis
    American Society for Microbiology ; 2010
    In:  Infection and Immunity Vol. 78, No. 12 ( 2010-12), p. 5022-5032
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 78, No. 12 ( 2010-12), p. 5022-5032
    Abstract: Francisella tularensis is a highly virulent Gram-negative bacterium and is the etiological agent of the disease tularemia. IclR, a presumed transcriptional regulator, is required for full virulence of the animal pathogen, F. tularensis subspecies novicida U112 (53). In this study, we investigated the contribution of IclR to the intracellular growth, virulence, and gene regulation of human pathogenic F. tularensis subspecies. Deletion of iclR from the live vaccine strain (LVS) and SchuS4 strain of F. tularensis subsp. holarctica and F. tularensis subsp. tularensis , respectively, did not affect their abilities to replicate within macrophages or epithelial cells. In contrast to F. tularensis subsp. novicida iclR mutants, LVS and SchuS4 Δ iclR strains were as virulent as their wild-type parental strains in intranasal inoculation mouse models of tularemia. Furthermore, wild-type LVS and LVSΔ iclR were equally cytotoxic and induced equivalent levels of interleukin-1β expression by infected bone marrow-derived macrophages. Microarray analysis revealed that the relative expression of a limited number of genes differed significantly between LVS wild-type and Δ iclR strains. Interestingly, many of the identified genes were disrupted in LVS and SchuS4 but not in their corresponding F. tularensis subsp. novicida U112 homologs. Thus, despite the impact of iclR deletion on gene expression, and in contrast to the effects of iclR deletion on F. tularensis subsp. novicida virulence, IclR does not contribute significantly to the virulence or pathogenesis of F. tularensis LVS or SchuS4.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00544-10
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2010
    detail.hit.zdb_id: 1483247-1
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  • 4
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    The sodA gene of Haemophilus ducreyi encodes a hydrogen peroxide-inhibitable superoxide dismutase
    Elsevier BV ; 1998
    In:  Gene Vol. 207, No. 2 ( 1998-1), p. 251-257
    Details
    In: Gene, Elsevier BV, Vol. 207, No. 2 ( 1998-1), p. 251-257
    Type of Medium: Online Resource
    ISSN: 0378-1119
    URL: Article
    DOI: 10.1016/S0378-1119(97)00642-2
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1998
    detail.hit.zdb_id: 1491012-3
    SSG: 12
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  • 5
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    Examination of Early Interactions between Haemophilus ducreyi and Host Cells by Using Cocultured HaCaT Keratinocytes and Foreskin Fibroblasts
    American Society for Microbiology ; 1999
    In:  Infection and Immunity Vol. 67, No. 10 ( 1999-10), p. 5352-5360
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 67, No. 10 ( 1999-10), p. 5352-5360
    Abstract: Haemophilus ducreyi is the etiologic agent of chancroid, a sexually transmitted genital ulcer disease. Keratinocytes are likely the first cell type encountered by H. ducreyi upon infection of human skin; thus, the interaction between H. ducreyi and keratinocytes is probably important for the ability of H. ducreyi to establish infection. We have used the HaCaT keratinocyte cell line grown in monolayers and in cocultures with HS27 fibroblasts to investigate H. ducreyi interactions with keratinocytes and the host-cell response to H. ducreyi infection. Using quantitative adherence and gentamicin protection assays, we determined that approximately 13% of H. ducreyi adhered to HaCaT cell monolayers, while only a small proportion (0.0052%) was intracellular. By transmission electron microscopy, we observed numerous H. ducreyi organisms adherent to but rarely within HaCaT cells cocultured with fibroblasts. Both live H. ducreyi and purified H. ducreyi lipooligosaccharide (LOS) induced significant interleukin 8 (IL-8) expression from HaCaT cell-HS27 cell cocultures. However, the level of IL-8 expression in response to LOS alone was not as pronounced. H. ducreyi LOS was a more potent inducer of IL-8 from cocultures than Escherichia coli lipopolysaccharide (LPS) at the same concentration, suggesting a unique effect of H. ducreyi LOS on cocultures. Neither live H. ducreyi nor purified H. ducreyi LOS or E. coli LPS induced tumor necrosis factor alpha expression from cocultures. H. ducreyi induced drastically different cytokine profiles from cocultures than from HS27 or HaCaT cells cultured separately. IL-8 expression by skin cells in response to H. ducreyi infection in vivo may be responsible for the massive influx of polymorphonuclear leukocytes and other inflammatory cells to the site of infection. This influx of inflammatory cells may be partly responsible for the tissue destruction characteristic of chancroid.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.67.10.5352-5360.1999
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1999
    detail.hit.zdb_id: 1483247-1
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  • 6
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    RipA, a Cytoplasmic Membrane Protein Conserved among Francisella Species, Is Required for Intracellular Survival
    American Society for Microbiology ; 2008
    In:  Infection and Immunity Vol. 76, No. 11 ( 2008-11), p. 4934-4943
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 76, No. 11 ( 2008-11), p. 4934-4943
    Abstract: Francisella tularensis is a highly virulent bacterial pathogen that invades and replicates within numerous host cell types, including macrophages and epithelial cells. In an effort to better understand this process, we screened a transposon insertion library of the F. tularensis live vaccine strain (LVS) for mutant strains that invaded but failed to replicate within alveolar epithelial cell lines. One such strain isolated from this screen contained an insertion in the gene FTL_1914, which is conserved among all sequenced Francisella species yet lacks significant homology to any gene with known function. A deletion strain lacking FTL_1914 was constructed. This strain did not replicate in either epithelial or macrophage-like cells, and intracellular replication was restored by the wild-type allele in trans . Based on the deletion mutant phenotype, FTL_1914 was termed ripA ( r equired for i ntracellular p roliferation, factor A ). Following uptake by J774.A1 cells, F. tularensis LVS ΔripA colocalized with LAMP-1 then escaped the phagosome at the same rate and frequency as wild-type LVS-infected cells. Electron micrographs of the F. tularensis LVS Δ ripA mutant demonstrated the reentry of the mutant bacteria into double membrane vacuoles characteristic of autophagosomes in a process that was not dependent on replication. The F. tularensis LVS ΔripA mutant was significantly impaired in its ability to persist in the lung and in its capacity to disseminate and colonize the liver and spleen in a mouse model of pulmonary tularemia. The RipA protein was expressed during growth in laboratory media and localized to the cytoplasmic membrane. Thus, RipA is a cytoplasmic membrane protein conserved among Francisella species that is required for intracellular replication within the host cell cytoplasm as well as disease progression, dissemination, and virulence.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00475-08
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2008
    detail.hit.zdb_id: 1483247-1
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  • 7
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    Francisella tularensis Replicates within Alveolar Type II Epithelial Cells In Vitro and In Vivo following Inhalation
    American Society for Microbiology ; 2007
    In:  Infection and Immunity Vol. 75, No. 2 ( 2007-02), p. 1034-1039
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 75, No. 2 ( 2007-02), p. 1034-1039
    Abstract: Francisella tularensis replicates in macrophages and dendritic cells, but interactions with other cell types have not been well described. F. tularensis LVS invaded and replicated within alveolar epithelial cell lines. Following intranasal inoculation of C57BL/6 mice, Francisella localized to the alveolus and replicated within alveolar type II epithelial cells.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.01254-06
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2007
    detail.hit.zdb_id: 1483247-1
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  • 8
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    Genome-Wide Identification of Francisella tularensis Virulence Determinants
    American Society for Microbiology ; 2007
    In:  Infection and Immunity Vol. 75, No. 6 ( 2007-06), p. 3089-3101
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 75, No. 6 ( 2007-06), p. 3089-3101
    Abstract: Francisella tularensis is a gram-negative pathogen that causes life-threatening infections in humans and has potential for use as a biological weapon. The genetic basis of the F. tularensis virulence is poorly understood. This study screened a total of 3,936 transposon mutants of the live vaccine strain for infection in a mouse model of respiratory tularemia by signature-tagged mutagenesis. We identified 341 mutants attenuated for infection in the lungs. The transposon disruptions were mapped to 95 different genes, virtually all of which are also present in the genomes of other F. tularensis strains, including human pathogenic F. tularensis strain Schu S4. A small subset of these attenuated mutants carried insertions in the genes encoding previously known virulence factors, but the majority of the identified genes have not been previously linked to F. tularensis virulence. Among these are genes encoding putative membrane proteins, proteins associated with stress responses, metabolic proteins, transporter proteins, and proteins with unknown functions. Several attenuated mutants contained disruptions in a putative capsule locus which partially resembles the poly-γ-glutamate capsule biosynthesis locus of Bacillus anthracis , the anthrax agent. Deletional mutation analysis confirmed that this locus is essential for F. tularensis virulence.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.01865-06
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2007
    detail.hit.zdb_id: 1483247-1
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  • 9
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    The Haemophilus ducreyi Serum Resistance Antigen DsrA Confers Attachment to Human Keratinocytes
    American Society for Microbiology ; 2002
    In:  Infection and Immunity Vol. 70, No. 11 ( 2002-11), p. 6158-6165
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 70, No. 11 ( 2002-11), p. 6158-6165
    Abstract: Haemophilus ducreyi is the etiologic agent of the sexually transmitted genital ulcer disease chancroid. H. ducreyi serum resistance protein A (DsrA) is a member of a family of multifunctional outer membrane proteins that are involved in resistance to killing by human serum complement. The members of this family include YadA of Yersinia species, the UspA proteins of Moraxella catarrhalis , and the Eib proteins of Escherichia coli. The role of YadA, UspA1, and UspA2H as eukaryotic cell adhesins and the function of UspA2 as a vitronectin binder led to our investigation of the cell adhesion and vitronectin binding properties of DsrA. We found that DsrA was a keratinocyte-specific adhesin as it was necessary and sufficient for attachment to HaCaT cells, a keratinocyte cell line, but was not required for attachment to HS27 cells, a fibroblast cell line. We also found that DsrA was specifically responsible for the ability of H. ducreyi to bind vitronectin. We then theorized that DsrA might use vitronectin as a bridge to bind to human cells, but this hypothesis proved to be untrue as eliminating HaCaT cell binding of vitronectin with a monoclonal antibody specific to integrin α v β 5 did not affect the attachment of H. ducreyi to HaCaT cells. Finally, we wanted to examine the importance of keratinocyte adhesion in chancroid pathogenesis so we tested the wild-type and dsrA mutant strains of H. ducreyi in our swine models of chancroid pathogenesis. The dsrA mutant was less virulent than the wild type in both the normal and immune cell-depleted swine models of chancroid infection.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.70.11.6158-6165.2002
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2002
    detail.hit.zdb_id: 1483247-1
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  • 10
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    Author response
    eLife Sciences Publications, Ltd ; 2016
    In:  eLife Vol. 5 ( 2016-01-23)
    Details
    In: eLife, eLife Sciences Publications, Ltd, Vol. 5 ( 2016-01-23)
    Abstract: Many of the bacteria that are able to cause disease in humans and other animals are able to grow inside their host’s cells. In doing so, these bacteria can avoid being recognized and killed by the host’s immune system. However, the ability of the bacteria to grow within the cell is constrained by the limited space and nutrients that are available inside the infected cell. The current theory is that most of these bacteria eventually kill the cell they have infected and are released into the body so that they can infect other host cells. However, since some host cells can exchange material with their neighbors, it is also possible that the bacteria may be able to travel directly between host cells without leaving the safety of the cell environment. Macrophages are immune cells that patrol the body to identify and destroy damaged host cells, bacteria and other microbes. Macrophages are also able to interact with neighboring healthy cells through a process called trogocytosis (“trogo” is essentially Greek for nibble). During this process, the membranes of the two participating cells briefly fuse and some of the proteins in the membranes are transferred from one cell to the other. Afterwards, the two cells separate but retain the membrane proteins they acquired from the other cell. The purpose of trogocytosis is poorly understood, but it is thought to help the host to develop immune responses against microbes and tumors. Steele et al. investigated whether infected mouse and human cells can transfer bacteria to healthy macrophages during trogocytosis. The experiments show that two types of bacteria – called Francisella tularensis and Salmonella enterica – can transfer from infected cells to macrophages via trogocytosis. Furthermore, the cells of mice infected with F. tularensis were more likely to undergo trogocytosis, which suggests that the bacterium may promote and use this process to spread throughout tissues in the body. Together, Steele et al.’s finding show that some bacteria can hijack a naturally occurring cellular process to move between host cells without re-entering the space that surrounds cells, or damaging either the donor or recipient cell.The next steps following on from this work are to find out how much trogocytosis contributes to the spread and progression of disease. A future goal is to understand the molecular mechanism of trogocytosis so it may be possible to develop drugs that can inhibit the spread of the bacteria in patients.
    Type of Medium: Online Resource
    ISSN: 2050-084X
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    DOI: 10.7554/eLife.10625
    DOI: 10.7554/eLife.10625.001
    DOI: 10.7554/eLife.10625.002
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    DOI: 10.7554/eLife.10625.017
    DOI: 10.7554/eLife.10625.018
    DOI: 10.7554/eLife.10625.019
    Language: English
    Publisher: eLife Sciences Publications, Ltd
    Publication Date: 2016
    detail.hit.zdb_id: 2687154-3
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