ArticleCellular microbiology2013
Innate immune recognition of flagellin limits systemic persistence of Brucella.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- To Move or Not to Move: When and How Bacteria Suppress Flagellar Motility.Molecular microbiology · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Review
- Brucella abortus interferes with the inflammatory response and tissue repair in mice.Scientific reports · 2025Article
- Brucellosis in the omics era: integrative perspectives on Brucella genomic architecture, host-pathogen interactions, and disease dynamics.World journal of microbiology & biotechnology · 2025Review
- Brucellosis: Bacteriology, pathogenesis, epidemiology and role of the metallophores in virulence: a review.Frontiers in cellular and infection microbiology · 2025Review
- Beyond survival to domination:Frontiers in microbiology · 2025Review
- Review
- Review
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Virulence factors perforate the pathogen-containing vacuole to signal efferocytosis.Cell host & microbe · 2022Article
- Review
- Undercover Agents of Infection: The Stealth Strategies of T4SS-Equipped Bacterial Pathogens.Toxins · 2021Review
- Design of a new multi-epitope vaccine againstEpidemiology and infection · 2021Article
- Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- RNA-Seq Analysis Reveals the Role of Omp16 inFrontiers in veterinary science · 2021Article
- The Role of Neutrophils in Brucellosis.Microbiology and molecular biology reviews : MMBR · 2020Review
- The Three Flagellar Loci ofFrontiers in veterinary science · 2020Article
- The Role of the Flagellar Protein FlgJ in the Virulence ofFrontiers in cellular and infection microbiology · 2020Article
- The relationship between caspase-1 related inflammasome expression and serum inflammatory cytokine levels during acute brucellosis.Northern clinics of Istanbul · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Brucella are facultative intracellular bacteria that cause chronic infections by limiting innate immune recognition. It is currently unknown whether Brucella FliC flagellin, the monomeric subunit of flagellar filament, is sensed by the host during infection. Here, we used two mutants of Brucella melitensis, either lacking or overexpressing flagellin, to show that FliC hinders bacterial replication in vivo. The use of cells and mice genetically deficient for different components of inflammasomes suggested that FliC was a target of the cytosolic innate immune receptor NLRC4 in vivo but not in macrophages in vitro where the response to FliC was nevertheless dependent on the cytosolic adaptor ASC, therefore suggesting a new pathway of cytosolic flagellin sensing. However, our work also suggested that the lack of TLR5 activity of Brucella flagellin and the regulation of its synthesis and/or delivery into host cells are both part of the stealthy strategy of Brucella towards the innate immune system. Nevertheless, as a flagellin-deficient mutant of B. melitensis wasfound to cause histologically demonstrable injuries in the spleen of infected mice, we suggested that recognition of FliC plays a role in the immunological stand-off between Brucella and its host, which is characterized by a persistent infection with limited inflammatory pathology.
Indexed as
Identifiers
What OpenQuestion holds
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.