19 research outputs found
Intoxicação por Senecio spp. em bovinos no Rio Grande do Sul: condições ambientais favoráveis e medidas de controle
Este trabalho teve por objetivo revisar os principais aspectos da intoxicação por Senecio spp. no Rio Grande do Sul no que se refere à patologia, patogenia e epidemiologia dessa importante causa de morte em bovinos nesse Estado. Foram abordados, também, os principais fatores climáticos e ambientais que aparentemente favorecem a emergência e o estabelecimento da planta e a ocorrência da intoxicação, que tem aumentado a sua frequência nos últimos anos no Estado, e as possÃveis formas de controle da planta incluindo o manejo correto do solo e a utilização de espécies domésticas menos susceptÃveis nas áreas invadidas
Genetic engineering of Streptococcus gordonii for the simultaneous display of two heterologous proteins at the bacterial surface
The Gram-positive bacterium Streptococcus gordonii has been genetically engineered to allow the simultaneous expression of two heterologous proteins at the cell surface. A family of recombinant streptococci displaying two different antigens was constructed. All the strains were genetically stable and expressed both proteins at the surface of the same bacterial cell. S. gordonii co-expressing the immunomodulating molecule LTB (B monomer of Escherichia coli heat-labile toxin) and the V3 domain of HIV-1 gp120 were inoculated subcutaneously to BALB/c mice. Animals were capable of responding to both antigens, producing LTB- and V3-specific serum IgG. The V3-specific IgG titer was four-fold higher in mice immunised with the double protein-expressing bacteria, as compared to control animals inoculated either with S. gordonii expressing the V3 domain alone or with a mixture of the two strains expressing LTB and V3, separately. Therefore, LTB was able to potentiate the antibody response towards the V3 domain, and this effect was observed only when LTB was co-expressed on the same bacterial cell
The HrpB-HrpA two-partner secretion system is essential for intracellular survival of Neisseria meningitidis
In this study we used HeLa cells to investigate the role of the HrpB-HrpA two-partner secretion (TPS) system in the meningococcal infection cycle. Although there is evidence that several pathogenic microorganisms may use TPS systems to colonize epithelial surfaces, the meningococcal HrpB-HrpA TPS system was not primarily involved in adhesion to or invasion of HeLa cells. Instead, this system was essential for intracellular survival and escape from infected cells. Gentamicin protection assays, immunofluorescence and transmission electron microscopy analyses demonstrated that, in contrast to the wild-type strain, HrpB-HrpA-deficient mutants were primarily confined to late endocytic vacuoles and trapped in HeLa cells. Haemolytic tests using human erythrocytes suggested that the secreted HrpA proteins could act as manganese-dependent lysins directly involved in mediating vacuole escape. In addition, we demonstrated that escape of wild-type meningococci from infected cells required the use of an intact tubulin cytoskeleton and that the hrpB-hrpA genes, which are absent in other Neisseria spp., were upregulated during infection. © 2008 Blackwell Publishing Ltd
Therapy of mucosal candidiasis by expression of an anti-idiotype in human commensal bacteria.
Two recombinant strains of Streptococcus gordonii, secreting or displaying a microbicidal single-chain antibody (H6), and stably colonizing rat vagina, were used to treat an experimental vaginitis caused by Candida albicans. A post-challenge intravaginal delivery of the H6-secreting strain was as efficacious as fluconazole in rapidly abating the fungal burden. Three weeks after challenge, 75% and 37.5% of the rats treated with the H6-secreting or displaying bacteria, respectively, were cured of the infection, which persisted in 100% of the animals treated with a S. gordonii strain expressing an irrelevant single-chain antibody. Thus, a human commensal bacterium can be suitably engineered to locally release a therapeutic antibody fragment