ArticleFrontiers in cellular and infection microbiology2012
Host interferon-γ inducible protein contributes to Brucella survival.
Article in Frontiers in cellular and infection microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Phylogeny-guided multi-epitope vaccine design targeting conserved and divergent regions of Brucella OMP2, OMP25, and OMP31: an immunoinformatics study.BMC immunology · 2026Article
- The Lpp-OmpA-BtaE fusion protein causes a protective immune response against Brucella melitensis in mice.Scientific reports · 2025Article
- Imipramine-induced immunomodulation and intracellular growth inhibition duringFrontiers in veterinary science · 2025Article
- Intraperitoneal Treatment of Cambinol, a Synthetic SIRT1 and SIRT2 Inhibitory Compound, ExacerbatesMicroorganisms · 2024Article
- Concomitant Treatment with Doxycycline and Rifampicin in Balb/c Mice Infected withPharmaceuticals (Basel, Switzerland) · 2024Article
- Comparison of cytokine immune responses to Brucella abortus and Yersinia enterocolitica serotype O:9 infections in BALB/c mice.Infection and immunity · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Brucella spp. are highly adapted intracellular pathogens of mammals that cause chronic infections while surving and replicating in host monocytes and macrophages. Although monocytes are normally susceptible to infection, pretreatment with pro-inflammatory cytokine interferon-γ (IFN-γ) activates cellular defense mechanisms that increase intracellular killing of Brucella and prevents bacterial replication. We examined the contribution of the IFN-γ inducible GTPase, LRG-47, to B. abortus 2308 infection in in vitro and in vivo murine models. Infecting non-activated macrophages from LRG-47(-/-) mice revealed that loss of this host protein negatively effected the intracellular survival and replication of IgG opsonized B. abortus. In contrast, survival and replication of non-opsonized B. abortus was the same in both C57/B6 and LRG-47(-/-) peritoneal macrophages. Following IFN-γ activation of LRG-47(-/-) monocytes, IgG opsonized B. abortus survived better than non-opsonized bacteria. The differential fate of opsonized and non-opsonized B. abortus was only observed in macrophages collected from LRG-47(-/-) mice. Given the specific nature of the relationship between this host protein and the mechanism of Brucella internalization, LRG-47(-/-) mice were infected with B. abortus to assess whether the loss of the lrg47 protein would affect the ability of the bacteria to colonize or persist within the host. B. abortus were able to establish and maintain similar numbers of bacteria in both C57/B6 mice and LRG-47(-/-) through 3 weeks post intraperitoneal infection. By 9 weeks p.i. fewer B. abortus were recovered from LRG-47(-/-) mice than controls, suggesting that the host protein has a positive role in maintaining long term persistence of the bacteria within the host. These observations demonstrating a positive role for a host IFN-γ induced protein defense protein has yet to be reported. These results provide interesting insight into the complex interaction between Brucella and their host.
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Registered trials
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