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Intracellular killing of Brucella melitensis within mouse peritoneal macrophages: influence of treatment with
Abstract:
The aggregation and condensation of ribosomes and the disjunction of the cell-wall membranous system are the ultrastructural alterations caused by rifampicin on B. melitensis cultured in Brucella-Broth medium. Our ultrastructural researches carried out on mouse peritoneal macrophages infected with B. melitensis and treated with rifampicin (1 microgram/ml) have demonstrated that vacuoles containing B. melitensis which had been damaged by the drug fuse with lysosomes. On the contrary vacuoles containing undamaged and viable Brucellae showed markedly impaired lysosomal fusion.
Insights
Rifampicin damages Brucella melitensis (B. melitensis) ribosomes and cell walls. Damaged bacteria within vacuoles fuse with lysosomes in macrophages, unlike healthy bacteria.
Area of Science:
- Microbiology
- Cell Biology
- Drug Discovery
Background:
- Brucella melitensis (B. melitensis) is a facultative intracellular bacterium causing brucellosis.
- Understanding the host-pathogen interactions and the effects of antibiotics on B. melitensis is crucial for treatment.
- Rifampicin is a key antibiotic used against brucellosis.
Purpose of the Study:
- To investigate the ultrastructural effects of rifampicin on B. melitensis.
- To examine the interaction between rifampicin-treated B. melitensis and host macrophages.
Main Methods:
- B. melitensis was cultured in Brucella-Broth medium and observed for ultrastructural changes.
- Mouse peritoneal macrophages were infected with B. melitensis and treated with rifampicin (1 microgram/ml).
- Transmission electron microscopy was used to analyze the ultrastructure of bacteria and host cells.
Main Results:
- Rifampicin induced aggregation and condensation of ribosomes and disjunction of the cell-wall membranous system in B. melitensis.
- Vacuoles containing rifampicin-damaged B. melitensis exhibited fusion with lysosomes in macrophages.
- Vacuoles containing undamaged, viable B. melitensis showed impaired lysosomal fusion.
Conclusions:
- Rifampicin causes significant ultrastructural damage to B. melitensis.
- The drug enhances the susceptibility of B. melitensis to lysosomal degradation within macrophages.
- These findings provide insights into the mechanism of action of rifampicin against B. melitensis infections.