ArticleJournal of leukocyte biology2016
TLR9 is required for MAPK/NF-κB activation but does not cooperate with TLR2 or TLR6 to induce host resistance to Brucella abortus.
Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Gut metabolites and inflammation factors in non-alcoholic fatty liver disease: A systematic review and meta-analysis.Scientific reports · 2020Pooled it
- Pathogenicity and virulence ofVirulence · 2025Review
- Central Role of Toll-like Receptor-9 Gene Function in Inflammation-Mediated Neuronal Plasticity: Implications for Long-Term Memory Development.Molecular neurobiology · 2025Review
- The impact of STING signaling on myeloid cells highlights macrophages as the major player in controllingFrontiers in immunology · 2025Article
- Potential mechanisms of natural metabolites and botanical drugs foumulae for the treatment of non-alcoholic fatty liver disease: targeting the gut microbiota to modulate the immune system.Frontiers in pharmacology · 2025Review
- Review
- ZBP1 sensesFrontiers in immunology · 2024Article
- Review
- The Intersection of COVID-19 and Metabolic-Associated Fatty Liver Disease: An Overview of the Current Evidence.Viruses · 2023Review
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- Review
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Article
- Protection of toll-like receptor 9 against lipopolysaccharide-induced inflammation and oxidative stress of pulmonary epithelial cells via MyD88-mediated pathways.Physiological research · 2022Article
- Caspase-8 but not caspase-7 influences inflammasome activation to act in control ofFrontiers in microbiology · 2022Article
- How the crosstalk between innate immune sensors and metabolic pathways affect the outcome ofFrontiers in microbiology · 2022Article
- Galectin-3 regulates proinflammatory cytokine function and favours Brucella abortus chronic replication in macrophages and mice.Cellular microbiology · 2021Article
- MyD88-Dependent Glucose Restriction and Itaconate Production Control Brucella Infection.Infection and immunity · 2021Article
- STING regulates metabolic reprogramming in macrophages via HIF-1α during Brucella infection.PLoS pathogens · 2021Article
- Gut microbiota and their metabolites in the progression of non-alcoholic fatty liver disease.Hepatoma research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Brucella abortus is a Gram-negative intracellular bacterial pathogen that causes a zoonosis of worldwide occurrence, leading to undulant fever in humans and abortion in domestic animals. B. abortus is recognized by several pattern-recognition receptors triggering pathways during the host innate immune response. Therefore, here, we determined the cooperative role of TLR9 with TLR2 or TLR6 receptors in sensing Brucella Furthermore, we deciphered the host innate immune response against B. abortus or its DNA, emphasizing the role of TLR9-MAPK/NF-κB signaling pathways in the production of proinflammatory cytokines. TLR9 is required for the initial host control of B. abortus, but this TLR was dispensable after 6 wk of infection. The susceptibility of TLR9(-/-)-infected animals to Brucella paralleled with lower levels of IFN-γ produced by mouse splenocytes stimulated with this pathogen compared with wild-type cells. However, no apparent cooperative interplay was observed between TLR2-TLR9 or TLR6-TLR9 receptors to control infection. Moreover, B. abortus or its DNA induced activation of MAPK/NF-κB pathways and production of IL-12 and TNF-α by macrophages partially dependent on TLR9 but completely dependent on MyD88. In addition, B. abortus-derived CpG oligonucleotides required TLR9 to promote IL-12 and TNF-α production by macrophages. By confocal microscopy, we demonstrated that TLR9 redistributed and colocalized with lysosomal-associated membrane protein-1 upon Brucella infection. Thus, B. abortus induced TLR9 traffic, leading to cell signaling activation and IL-12 and TNF-α production. Although TLR9 recognized Brucella CpG motifs, our results suggest a new pathway of B. abortus DNA-activating macrophages independent of TLR9.
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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.