Isogenic Murine Model
Mostrando 1-12 de 40 artigos, teses e dissertações.
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1. Paracoccidioidomicose: acompanhamento de parâmetros de imunidade adquirida e do estado de ativação de fagócitos em camundongos isogênicos suscetíveis submetidos à terapia antifúngica. / Paracoccidioidomycosis: follow up of acquired immunity parameters and of the activation state of phagocytes in susceptible isogenic mice submitted to the antifungal therapy.
Os efeitos da administração de anfotericina B a camundongos suscetíveis ao P. brasiliensis foram avaliados. A L-AmB reverte o padrão de suscetibilidade para o de resistência de forma mais eficiente do que a c-AmB, como observado na quantificação de UFC, NO e IgG2b. Porém, os níveis de TNF-a, IL-12, IFN-g, GM-CSF, IgG total, IgM, IgG1, IgG2a e IgA n�
Publicado em: 2009
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2. Lagochilascaríase Experimental em Camundongos A/J e B10.A
Lagochilascariasis is an infection caused by a parasite from the genus Lagochilascaris and the species is Lagochilascaris minor Leiper 1909 Campos et al (1992) described its experimental evolutive cycle using a model constituted by mice as intermediate hosts and by domestic cats as definitive hosts The availability of murine strains with different genetic ch
Publicado em: 2006
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3. Lagochilascaríase Experimental em Camundongos A/J e B10.A
Lagochilascariasis is an infection caused by a parasite from the genus Lagochilascaris and the species is Lagochilascaris minor Leiper 1909 Campos et al (1992) described its experimental evolutive cycle using a model constituted by mice as intermediate hosts and by domestic cats as definitive hosts The availability of murine strains with different genetic ch
Publicado em: 2006
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4. Role of RgpA, RgpB, and Kgp Proteinases in Virulence of Porphyromonas gingivalis W50 in a Murine Lesion Model
Extracellular Arg-x- and Lys-x-specific cysteine proteinases are considered important virulence factors and pathogenic markers for Porphyromonas gingivalis, a bacterium implicated as a major etiological agent of chronic periodontitis. Three genes. rgpA, rgpB, and kgp, encode an Arg-x-specific proteinase and adhesins (RgpA), an Arg-x-specific proteinase (RgpB
American Society for Microbiology.
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5. The HtrA stress response protease contributes to resistance of Brucella abortus to killing by murine phagocytes.
Compared with virulent Brucella abortus 2308, the isogenic htrA mutant PHE1 shows decreased resistance to killing by cultured murine neutrophils and macrophages and significant attenuation during the early stages of infection in the BALB/c mouse model. These findings further define the contributions of the htrA gene product to the pathogenesis of B. abortus
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6. In Vitro and In Vivo Characterization of Helicobacter hepaticus Cytolethal Distending Toxin Mutants
Helicobacter hepaticus expresses a member of the cytolethal distending toxin (CDT) family of bacterial cytotoxins. To investigate the role of CDT in the pathogenesis of H. hepaticus, transposon mutagenesis was used to generate a series of isogenic mutants in and around the cdtABC gene cluster. An H. hepaticus transposon mutant with a disrupted cdtABC coding
American Society for Microbiology.
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7. The lpf fimbrial operon mediates adhesion of Salmonella typhimurium to murine Peyer's patches.
We investigated the role of the Salmonella typhimurium fimbrial operon formed by the genes lpfABCDE in infection of mice. A mutant in lpfC, the gene encoding the fimbrial outer membrane usher, had an approximately 5-fold increased 50% lethal dose when administered orally to mice. When mice were infected with a mixture of the lpfC mutant and isogenic wild-typ
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8. Activity of pyrazinamide in a murine model against Mycobacterium tuberculosis isolates with various levels of in vitro susceptibility.
The activity of pyrazinamide (PZA) against eight isolates of Mycobacterium tuberculosis in a murine infection model was evaluated. M. tuberculosis isolates with various degrees of in vitro susceptibility to PZA (MIC range, 32 to > 2,048 micrograms/ml) were used. Four-week-old female mice were infected intravenously with approximately 10(7) viable M. tubercul
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9. Intact Purine Biosynthesis Pathways Are Required for Wild-Type Virulence of Brucella abortus 2308 in the BALB/c Mouse Model
Brucella abortus 2308 derivatives with mini-Tn5 insertions in purE, purL, and purD display significant attenuation in the BALB/c mouse model, while isogenic mutants with mini-Tn5 insertions in pheA, trpB, and dagA display little or no attenuation in cultured murine macrophages or mice. These experimental findings confirm the importance of the purine biosynth
American Society for Microbiology.
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10. Caspofungin Resistance in Candida albicans: Correlating Clinical Outcome with Laboratory Susceptibility Testing of Three Isogenic Isolates Serially Obtained from a Patient with Progressive Candida Esophagitis
A patient with azole-refractory thrush-esophagitis responded initially to caspofungin, but the treatment eventually failed. In a murine model, caspofungin was effective against two early isolates for which the MICs of caspofungin were low, but it was less effective against a late isolate for which the MIC of caspofungin was greater. We concluded that there i
American Society for Microbiology.
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11. The Siderophore 2,3-Dihydroxybenzoic Acid Is Not Required for Virulence of Brucella abortus in BALB/c Mice
2,3-Dihydroxybenzoic acid (DHBA) is the only siderophore described for Brucella, and previous studies suggested that DHBA might contribute to the capacity of these organisms to persist in host macrophages. Employing an isogenic siderophore mutant (ΔentC) constructed from virulent Brucella abortus 2308, however, we found that production of DHBA is not requir
American Society for Microbiology.
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12. Sigma Factor B and RsbU Are Required for Virulence in Staphylococcus aureus-Induced Arthritis and Sepsis
The prototype Staphylococcus aureus strain 8325-4 produces high levels of hemolysins and proteases. Recently it has been shown that this property depends on a deficiency of sigma factor B (SigB) activity controlling the activation of regulatory genes such as agr and sarA. SigB deficiency is in turn due to a mutation in the rsbU gene, which is required for po
American Society for Microbiology.