ArticleThe Journal of experimental medicine2003
Brucella evades macrophage killing via VirB-dependent sustained interactions with the endoplasmic reticulum.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers.
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Who cites it
297 citing papers in PubMed, 539 citations in OpenAlex.
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- Brucella Omp25 activates the unfolded protein response to promote intracellular proliferation and inflammation.The Journal of biological chemistry · 2026Article
- Comprehensive genomic identification of essential genes required for Brucella melitensis intracellular survival during macrophage infection.Scientific reports · 2026Article
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- Complementary Use of Probiotics and Their Antimicrobial Proteins in Brucellosis: A Comprehensive Review of Mechanisms and Clinical Benefits.Probiotics and antimicrobial proteins · 2026Review
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- A previously uncharacterized Fur-family metalloregulator integrates iron- and manganese-sensing to control virulence gene regulatory networks in Brucella.Scientific reports · 2025Article
237 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intracellular pathogen Brucella is the causative agent of brucellosis, a worldwide zoonosis that affects mammals, including humans. Essential to Brucella virulence is its ability to survive and replicate inside host macrophages, yet the underlying mechanisms and the nature of the replicative compartment remain unclear. Here we show in a model of Brucella abortus infection of murine bone marrow-derived macrophages that a fraction of the bacteria that survive an initial macrophage killing proceed to replicate in a compartment segregated from the endocytic pathway. The maturation of the Brucella-containing vacuole involves sustained interactions and fusion with the endoplasmic reticulum (ER), which creates a replicative compartment with ER-like properties. The acquisition of ER membranes by replicating Brucella is independent of ER-Golgi COPI-dependent vesicular transport. A mutant of the VirB type IV secretion system, which is necessary for intracellular survival, was unable to sustain interactions and fuse with the ER, and was killed via eventual fusion with lysosomes. Thus, we demonstrate that live intracellular Brucella evade macrophage killing through VirB-dependent sustained interactions with the ER. Moreover, we assign an intracellular function to the VirB system, as being required for late maturation events necessary for the biogenesis of an ER-derived replicative organelle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.