Kooperativer Bibliotheksverbund

Berlin Brandenburg

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  • 1
    Description: Indiana University-Purdue University Indianapolis (IUPUI) Borrelia burgdorferi, a bacterium which causes Lyme disease, is maintained in nature through a cycle involving two distinct hosts: a tick vector and a mammalian host. To adapt to these two diverse environments, B. burgdorferi undergoes dramatic alterations in its surface lipoprotein. Two essential lipoproteins, outer surface protein A (OspA) and outer surface protein C (OspC), are reciprocally regulated throughout the B. burgdorferi lifecycle. Very little is known about the regulation of OspA. These studies elucidate the regulatory mechanisms controlling the expression of OspA. Various truncations of the ospA promoter were created and then studied in our novel in vitro model of ospA repression or grown within the host-adapted model. A T-Rich region of the ospA promoter was determined to be a cis-element essential for both the full expression and full repression of ospA.
    Keywords: Borrelia Burgdorferi ; Ospa ; Outer Surface Lipoprotein A ; Borrelia Burgdorferi -- Research ; Lyme Disease ; Lyme Disease -- Molecular Aspects ; Spirochetes -- Molecular Aspects ; Lipoprotein A ; Host-Bacteria Relationships ; Bacteria -- Physiology ; Bacterial Cell Walls ; Bacterial Cell Surfaces
    Source: Networked Digital Library of Theses and Dissertations
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  • 2
    Description: Indiana University-Purdue University Indianapolis (IUPUI) Pseudomonas aeruginosa is a gram negative opportunistic pathogen with the capacity to cause serious disease by forming biofilms, most notably in the lungs of cystic fibrosis (CF) patients. Biofilms are communities of microorganisms that adhere to a solid surface, undergo global regulatory changes, secrete exopolysaccharides, and are innately antibiotic resistant. Virulence modulation is an important tool utilized by P. aeruginosa to propagate infection and biofilm formation in the CF airway. Many different virulence modulatory pathways and proteins have been identified including the protein, MgtE. MgtE has recently been discovered and has been implicated in virulence modulation, as an isogeneic mutation of mgtE leads to increased cytotoxicity. To further elucidate the role of MgtE in P. aerugionsa infections, transcriptional and translational regulation of this protein following antibiotic treatment has been explored. I have demonstrated that mgtE is transcriptionally upregulated following antibiotic treatment of most of the twelve antibiotics tested utilizing RT-PCR and QRT-PCR. A novel model system was employed, which utilizes cystic fibrosis bronchial epithelial (CFBE) cells homozygous for the ΔF508 mutation for these studies. This model system allows P. aeruginosa biofilms to form on CFBE cells modeling the P. aeruginosa in the CF airway. Translational effects of antibiotic treatment on MgtE have been attempted via Western blotting and cytotoxicity assays. Furthermore, to explore the possibility that mgtE is interacting with a known regulatory pathway, a transposon-mutant library was utilized and the regulatory proteins, AlgR and NarX, among others have been identified as possibly interacting with MgtE. Lastly, an MgtE homologue from Staphylococcus aureus was utilized to further demonstrate the virulence modulatory effects of MgtE by demonstrating the expression of the homologue results in decreased cytotoxicity, exactly like expression of the native P. aeruginosa MgtE. This research explores a newly discovered protein that impacts cytotoxicity and biofilm formation and provides valuable information about P. aeruginosa virulence.
    Keywords: Pseudomonas Aeruginosa ; Biofilm ; Cfbe Cell ; Algr ; Mgte ; Co-Culture ; Virulence ; Biofilms ; Pathogenic Microorganisms ; Bacteria -- Physiology ; Antibiotics -- Immunology ; Microbial Toxins ; Virulence (Microbiology) ; Cystic Fibrosis ; Pseudomonas Aeruginosa Infections -- Pathogenesis ; Pseudomonas Aeruginosa Infections -- Treatment ; Staphylococcus Aureus
    Source: Networked Digital Library of Theses and Dissertations
    Library Location Call Number Volume/Issue/Year Availability
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