Intracellular Passage Triggers a Molecular Response in Brucella abortus That Increases Its Infectiousness
| Autor: | Caterina Guzmán-Verri, Joselyn Méndez-Montoya, Edgardo Moreno, Esteban Chaves-Olarte, Carlos Chacón-Díaz, Marlen Cordero-Serrano, Pamela Altamirano-Silva |
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| Rok vydání: | 2021 |
| Předmět: |
Immunology
Brucella abortus Microbiology Bacterial Adhesion Type IV Secretion Systems chemistry.chemical_compound Brucellosis Bovine Bacterial Proteins Animals Secretion Pathogen Cellular Microbiology: Pathogen-Host Cell Molecular Interactions biology Virulence Endoplasmic reticulum Intracellular parasite Macrophages Autophagosomes Bafilomycin Gene Expression Regulation Bacterial biology.organism_classification Two-component regulatory system Cell biology Infectious Diseases chemistry Host-Pathogen Interactions Parasitology Cattle Intracellular Bacteria |
| Zdroj: | Infect Immun |
| ISSN: | 1098-5522 |
| Popis: | Brucella abortus is a facultatively extracellular-intracellular pathogen that encounters a diversity of environments within the host cell. We report that bacteria extracted from infected cells at late stages (48 h postinfection) of the intracellular life cycle significantly increase their ability to multiply in new target cells. This increase depends on early interaction with the cell surface, since the bacteria become more adherent and penetrate more efficiently than in vitro-grown bacteria. At this late stage of infection, the bacterium locates within an autophagosome-like compartment, facing starvation and acidic conditions. At this point, the BvrR/BvrS two-component system becomes activated, and the expression of the transcriptional regulator VjbR and the type IV secretion system component VirB increases. Using bafilomycin to inhibit BvrR/BvrS activation and using specific inhibitors for VjbR and VirB, we showed that the BvrR/BvrS and VjbR systems correlate with increased interaction with new host cells, while the VirB system does not. Bacteria released from infected cells under natural conditions displayed the same phenotype as intracellular bacteria. We propose a model in which the B. abortus BvrR/BvrS system senses the transition from its replicative niche at the endoplasmic reticulum to the autophagosome-like exit compartment. This activation leads to the expression of VirB, which participates in the release of the bacterium from the cells, and an increase in VjbR expression that results in a more efficient interaction with new host cells. |
| Databáze: | OpenAIRE |
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