RESUMO
Seven isolates of B. piliformis, the agent of Tyzzer's disease, obtained from various host species, were examined for cytotoxic activity by incubating culture filtrates on BRL 3A rat-hepatocyte and 3T3 mouse-fibroblast cell lines. One isolate exhibited cytopathic effects on BRL 3A cells, but not on 3T3 cells. Three other isolates were strongly cytotoxic for 3T3 cells but only slightly so for BRL 3A cells. The remaining three isolates showed no cytotoxicity for either cell line. The cytotoxic products were greater than 100 kDa in mol. wt, thermolabile, and partly destroyed by trypsin treatment. The data show that some B. piliformis isolates produce cytotoxic proteins, which may contribute to the pathogenesis of Tyzzer's disease.
Assuntos
Bacillus/patogenicidade , Citotoxinas/biossíntese , Fibroblastos/microbiologia , Fígado/microbiologia , Animais , Linhagem Celular , Enterite/microbiologia , Enterite/veterinária , Infecções por Bactérias Gram-Positivas/microbiologia , Infecções por Bactérias Gram-Positivas/veterinária , Células HeLa , Hepatite Animal/microbiologia , Humanos , Fígado/citologia , Síndrome , TemperaturaRESUMO
Glucocorticoid sensitive human lymphoblastoid cells CEM-C7 were examined for the effects of antiglucocorticoid RU38486 on the prevention of early dexamethasone-induced changes, including reduced cell growth, cell shrinkage and fragmentation, decrease in cell plating efficiency and incorporation of acetate into cellular lipids. When RU38486 was added no later than 24 hours after the addition of dexamethasone, it prevented the inhibition of [14C]acetate incorporation into nonsaponifiable lipids, partly reversed the decrease in plating efficiency and reduced cell fragmentation. In addition, the accumulation of dolichols in the nuclei of dexamethasone-treated cells was abolished by RU38486. These results indicate that glucocorticoid-induced changes in cellular lipids are receptor dependent and may be linked to the initiation of the apoptotic cascade.
