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All Library Books, journals and Electronic Records Telegrafenberg

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  • 1
    Electronic Resource
    Electronic Resource
    Bacterial copper- and zinc-cofactored superoxide dismutase contributes to the pathogenesis of systemic salmonellosis (1997)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 25 (1997), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Copper/zinc-cofactored superoxide dismutase ([Cu,Zn]-SOD) has been found in the periplasm of many bacterial species but its biological function is unknown. Here we report the cloning and characterization of sodC, encoding [Cu,Zn]-SOD, from Salmonella typhimurium. The predicted protein sequence shows only 58% identity to Escherichia coli SodC, and from this its chromosomal location and its immediate proximity to a phage gene, sodC, in Salmonella is speculated to have been acquired by bacteriophage-mediated horizontal transfer from an unknown donor. A sodC mutant of S. typhimurium was unimpaired on aerobic growth in rich medium but showed enhanced sensitivity in vitro to the microbicidal action of superoxide. S. typhimurium, S. choleraesuis and S. dublin sodC mutants showed reduced lethality in a mouse model of oral infection and persisted in significantly lower numbers in livers and spleens after intraperitoneal infection, suggesting that [Cu,Zn]-SOD plays a role in pathogenicity, protecting Salmonella against oxygen radical-mediated host defences. There was, however, no observable difference compared with wild type in the interaction of sodC mutants with porcine pleural, mouse peritoneal or J774 macrophages in vitro, perhaps reflecting the hierarchical capacity of different macrophage lines to kill Salmonella, the most efficient overwhelming the proposed protective effect of periplasmic SOD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.1997.5151877.x
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  • 2
    Electronic Resource
    Electronic Resource
    Identification and characterization of genomic loci unique to the Brazilian purpuric fever clonal group of H. influenzae biogroup aegyptius: functionality explored using meningococcal homology (2003)
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 47 (2003), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Brazilian purpuric fever (BPF) is a fulminant septicaemic infection of young children, caused by a clonal group of strains of Haemophilus influenzae biogroup aegyptius (Hae), an organism previously solely associated with conjunctivitis. Their special capacity to invade from the initial site of conjunctival infection is unexplained. A polymerase chain reaction (PCR)-amplified subtractive hybridization technique was used to identify genes specific to the BPF clonal group. A copy of bacteriophage HP1 and 46 further chromosomal loci were identified in the BPF but not in the conjunctivitis strain of Hae. Sixteen were characterized further, and one – encoding an analogue of the Legionella pneumophila epithelial cell entry-enhancing protein EnhC – was investigated in depth. Two genes, bpf001 and bpf002, unique to the BPF clonal group were identified between homologues of HI1276 and HI1277 in a complex locus close to H. influenzae genetic island 1, recently identified in pathogenic H. influenzae type b. Bpf001 encodes a protein homologous to EnhC and to the previously uncharacterized product of the meningococcal gene NMB0419. Functional studies of bpf001 proving intractable, NMB0419 was chosen as a surrogate for investigation and shown to modulate bacterial interaction with monolayers of human respiratory epithelial cells, promoting invasion, the first stage (for Hae) in the pathogenesis of BPF.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.2003.03359.x
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