ArticleFrontiers in cellular and infection microbiology2014
Coxiella burnetii lipopolysaccharide blocks p38α-MAPK activation through the disruption of TLR-2 and TLR-4 association.
Article in Frontiers in cellular and infection microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 21 citations in OpenAlex.
- Subverting Host Defense from Within: Innate Immune Modulation byPathogens (Basel, Switzerland) · 2026Review
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Review
- A Comprehensive Review of the Mechanisms of Human Q Fever: Pathogenesis and Pathophysiology.Pathogens (Basel, Switzerland) · 2025Review
- Coxiella burnetii as a model system for understanding host immune response against obligate intracellular, vacuolar pathogens.PLoS pathogens · 2025Article
- Susceptibility, Immunity, and Persistent Infection Drive Endemic Cycles of Coxiellosis on Dairy Farms.Animals : an open access journal from MDPI · 2024Article
- Article
- Multivalent vaccines demonstrate immunogenicity and protect againstFrontiers in immunology · 2023Article
- Primary Murine Macrophages as a Tool for Virulence Factor Discovery in Coxiella burnetii.Microbiology spectrum · 2022Article
- Natural Exposure- and Vaccination-Induced Profiles ofFrontiers in immunology · 2022Article
- Protective Effects ofInternational journal of molecular sciences · 2021Article
- Undercover Agents of Infection: The Stealth Strategies of T4SS-Equipped Bacterial Pathogens.Toxins · 2021Review
- Recent Advances on the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021Review
- Effect of algae or fish oil supplementation and porcine maternal stress on the adrenal transcriptome of male offspring fed a low-quality protein diet.Brain, behavior, & immunity - health · 2020Article
- aYAP modRNA reduces cardiac inflammation and hypertrophy in a murine ischemia-reperfusion model.Life science alliance · 2020Article
- "Hairiness" is a Facsimile of Reorganized Cytoskeletons: A Cytopathic Effect ofYonsei medical journal · 2019Review
- Article
- The roles of the TLR/NF‑κB signaling pathway in the mutual interactions between the lung and the large intestine.Molecular medicine reports · 2018Article
- Coxiella burnetii Lipopolysaccharide: What Do We Know?International journal of molecular sciences · 2017Review
- Analysis of the Caenorhabditis elegans innate immune response to Coxiella burnetii.Innate immunity · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To survive in macrophages, Coxiella burnetii hijacks the activation pathway of macrophages. Recently, we have demonstrated that C. burnetii, via its lipopolysaccharide (LPS), avoids the activation of p38α-MAPK through an antagonistic engagement of Toll-like receptor (TLR)-4. We investigated the fine-tuned mechanism leading to the absence of activation of the p38α-MAPK despite TLR-4 engagement. In macrophages challenged with LPS from the avirulent variants of C. burnetii, TLR-4 and TLR-2 co-immunoprecipitated. This association was absent in cells challenged by the LPS of pathogenic C. burnetii. The disruption makes TLRs unable to signal during the recognition of the LPS of pathogenic C. burnetii. The disruption of TLR-2 and TLR-4 was induced by the re-organization of the macrophage cytoskeleton by C. burnetii LPS. Interestingly, blocking the actin cytoskeleton re-organization relieved the disruption of the association TLR-2/TLR-4 by pathogenic C. burnetii and rescued the p38α-MAPK activation by C. burnetii. We elucidated an unexpected mechanism allowing pathogenic C. burnetii to avoid macrophage activation by the disruption of the TLR-2 and TLR-4 association.
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.