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  • 2000-2004  (6)
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  • 1
    Electronic Resource
    Electronic Resource
    MOLECULAR AND CELLULAR BASIS OF BARTONELLA PATHOGENESIS (2004)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Microbiology 58 (2004), S. 365-390 
    Details
    ISSN: 0066-4227
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology
    Notes: The genus Bartonella comprises several important human pathogens that cause a wide range of clinical manifestations: cat-scratch disease, trench fever, Carrion's disease, bacteremia with fever, bacillary angiomatosis and peliosis, endocarditis, and neuroretinitis. Common features of bartonellae include transmission by blood-sucking arthropods and the specific interaction with endothelial cells and erythrocytes of their mammalian hosts. For each Bartonella species, the invasion and persistent intracellular colonization of erythrocytes are limited to a specific human or animal reservoir host. In contrast, endothelial cells are target host cells in probably all mammals, including humans. Bartonellae subvert multiple cellular functions of human endothelial cells, resulting in cell invasion, proinflammatory activation, suppression of apoptosis, and stimulation of proliferation, which may cumulate in vasoproliferative tumor growth. This review summarizes our understanding of Bartonella-host cell interactions and the molecular mechanisms of bacterial virulence and persistence. In addition, current controversies and unanswered questions in this area are highlighted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.micro.58.030603.123700
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The VirB/VirD4 type IV secretion system of Bartonella is essential for establishing intraerythrocytic infection (2002)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 46 (2002), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Bartonellae are pathogenic bacteria uniquely adapted to cause intraerythrocytic infection in their human or animal reservoir host(s). Experimental infection of rats by Bartonella tribocorum revealed the initial colonization of a yet unidentified niche outside of circulating blood. This primary niche periodically seeds bacteria into the bloodstream, resulting in the invasion and persistent intracellular colonisation of erythrocytes. Here, this animal model was used for a genetic analysis of the virB locus (virB2-11) and the downstream located virD4 gene, which together encode a putative type IV secretion system (T4SS). A generic method for marker-less gene replacement allowed the generation of non-polar in-frame deletions in either virB4 or virD4. Both mutants were unable to cause bacteraemia, whereas complementation with the full-length genes in trans completely restored infectivity. Segregation analysis of the complementation plasmids further denoted that VirB4 and VirD4 are required at an early stage of the infection course before the onset of intraerythrocytic bacteraemia. This analysis of defined mutants in an in vivo model identified components of the VirB/VirD4 T4SS as the first bona fide pathogenicity factors in Bartonella.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.2002.03208.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The VirB type IV secretion system of Bartonella henselae mediates invasion, proinflammatory activation and antiapoptotic protection of endothelial cells (2004)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 52 (2004), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Bartonella henselae is an arthropod-borne zoonotic pathogen causing intraerythrocytic bacteraemia in the feline reservoir host and a broad range of clinical manifestations in incidentally infected humans. Remarkably, B. henselae can specifically colonize the human vascular endothelium, resulting in inflammation and the formation of vasoproliferative lesions known as bacillary angiomatosis and bacillary peliosis. Cultured human endothelial cells provide an in vitro system to study this intimate interaction of B. henselae with the vascular endothelium. However, little is known about the bacterial virulence factors required for this pathogenic process. Recently, we identified the type IV secretion system (T4SS) VirB as an essential pathogenicity factor in Bartonella, required  to  establish  intraerythrocytic  infection  in the mammalian reservoir. Here, we demonstrate that the VirB T4SS also mediates most of the virulence attributes associated  with  the  interaction  of B. henselae during the interaction with human endothelial cells. These include: (i) massive rearrangements of the actin cytoskeleton, resulting in the formation of bacterial aggregates and their internalization by the invasome structure; (ii) nuclear factor κB-dependent proinflammatory activation, leading to cell adhesion molecule expression and chemokine secretion, and (iii) inhibition of apoptotic cell death, resulting in enhanced endothelial cell survival. Moreover, we show that the VirB system mediates cytostatic and cytotoxic effects at high bacterial titres, which interfere with a potent VirB-independent mitogenic activity. We conclude that the VirB T4SS is a major virulence determinant of B. henselae, required for targeting multiple endothelial cell functions exploited by this vasculotropic pathogen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2958.2003.03964.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Genome-wide analysis of transcriptional hierarchy and feedback regulation in the flagellar system of Helicobacter pylori (2004)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 52 (2004), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Summary The flagellar system of Helicobacter pylori, which comprises more than 40 mostly unclustered genes, is essential for colonization of the human stomach mucosa. In order to elucidate the complex transcriptional circuitry of flagellar biosynthesis in H. pylori and its link to other cell functions, mutants in regulatory genes governing flagellar biosynthesis (rpoN, flgR, flhA, flhF, HP0244) and whole-genome microarray technology were used in this study. The regulon controlled by RpoN, its activator FlgR (FleR) and the cognate histidine kinase HP0244 (FleS) was characterized on a genome-wide scale for the first time. Seven novel genes (HP1076, HP1233, HP1154/1155, HP0366/367, HP0869) were identified as belonging to RpoN-associated flagellar regulons. The hydrogenase accessory gene HP0869 was the only annotated non-flagellar gene in the RpoN regulon. Flagellar basal body components FlhA and FlhF were characterized as functional equivalents to master regulators in H. pylori, as their absence led to a general reduction of transcripts in the RpoN (class 2) and FliA (class 3) regulons, and of 24 genes newly attributed to intermediate regulons, under the control of two or more promoters. FlhA- and FlhF-dependent regulons comprised flagellar and non-flagellar genes. Transcriptome analysis revealed that negative feedback regulation of the FliA regulon was dependent on the antisigma factor FlgM. FlgM was also involved in FlhA- but not FlhF-dependent feedback control of the RpoN regulon. In contrast to other bacteria, chemotaxis and flagellar motor genes were not controlled by FliA or RpoN. A true master regulator of flagellar biosynthesis is absent in H. pylori, consistent with the essential role of flagellar motility and chemotaxis for this organism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2958.2004.04006.x
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  • 5
    Electronic Resource
    Electronic Resource
    A bacterial conjugation machinery recruited for pathogenesis (2003)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 49 (2003), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Type IV secretion systems (T4SS) are multicomponent transporters of Gram-negative bacteria adapted to functions as diverse as DNA transfer in bacterial conjugation or the delivery of effector proteins into eukaryotic target cells in pathogenesis. The generally modest sequence conservation between T4SS may reflect their evolutionary distance and/or functional divergence. Here, we show that the establishment of intraerythrocytic parasitism by Bartonella tribocorum requires a putative T4SS, which shares an unprecedented level of sequence identity with the Trw conjugation machinery of the broad-host-range antibiotic resistance plasmid R388 (up to 80% amino acid identity for individual T4SS components). The highly conserved T4SS loci are collinear except for the presence of numerous tandem gene duplications in B. tribocorum, which mostly encode variant forms of presumed surface-exposed pilus subunits. Conservation is not only structural, but also functional: R388 mutated in either trwD or trwH encoding essential T4SS components could be trans-complemented for conjugation by the homologues of the B. tribocorum system. Conservation also includes the transcription regulatory circuit: both T4SS loci encode a highly homologous and interchangeable KorA/KorB repressor system that negatively regulates the expression of all T4SS components. This striking example of adaptive evolution reveals the capacity of T4SS to assume dedicated functions in either DNA transfer or pathogenesis over rather short evolutionary distance and implies a novel role for the conjugation systems of widespread broad-host-range plasmids in the evolution of bacterial pathogens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.2003.03650.x
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  • 6
    Electronic Resource
    Electronic Resource
    Role of PlGF in the intra- and intermolecular cross talk between the VEGF receptors Flt1 and Flk1 (2003)
    [s.l.] : Nature Publishing Group
    Nature medicine 9 (2003), S. 936-943 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Therapeutic angiogenesis is likely to require the administration of factors that complement each other. Activation of the receptor tyrosine kinase (RTK) Flk1 by vascular endothelial growth factor (VEGF) is crucial, but molecular interactions of other factors with VEGF and Flk1 have been studied to ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm884
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