ArticleInfection and immunity2009
Live Borrelia burgdorferi spirochetes elicit inflammatory mediators from human monocytes via the Toll-like receptor signaling pathway.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Host-microbe interaction-mediated resistance to DSS-induced inflammatory enteritis in sheep.Microbiome · 2024Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Correlation between COVID-19 severity and previous exposure of patients to Borrelia spp.Scientific reports · 2022Article
- Host-microbiota interaction-mediated resistance to inflammatory bowel disease in pigs.Microbiome · 2022Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Effect ofAntibiotics (Basel, Switzerland) · 2020Article
- The Lyme disease bacterium, Borrelia burgdorferi, stimulates an inflammatory response in human choroid plexus epithelial cells.PloS one · 2020Article
- Investigating disease severity in an animal model of concurrent babesiosis and Lyme disease.International journal for parasitology · 2019Review
- Activation of the Innate Immune System by Treponema denticola Periplasmic Flagella through Toll-Like Receptor 2.Infection and immunity · 2018Article
- Article
- Early Gut Microbiota Intervention Suppresses DSS-Induced Inflammatory Responses by Deactivating TLR/NLR Signalling in Pigs.Scientific reports · 2017Article
- The Jarisch-Herxheimer Reaction After Antibiotic Treatment of Spirochetal Infections: A Review of Recent Cases and Our Understanding of Pathogenesis.The American journal of tropical medicine and hygiene · 2017Review
- Spirochetal Lipoproteins and Immune Evasion.Frontiers in immunology · 2017Review
- Differentiated THP-1 Cells Exposed to Pathogenic and Nonpathogenic Borrelia Species Demonstrate Minimal Differences in Production of Four Inflammatory Cytokines.Vector borne and zoonotic diseases (Larchmont, N.Y.) · 2016Article
- The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability.Molecular neurobiology · 2016Review
- Toll-Like Receptor 1/2 and 5 Ligands Enhance the Expression of Cyclin D1 and D3 and Induce Proliferation in Mantle Cell Lymphoma.PloS one · 2016Article
- Inflammatory mediator release from primary rhesus microglia in response to Borrelia burgdorferi results from the activation of several receptors and pathways.Journal of neuroinflammation · 2015Article
- Borrelia burgdorferi RNA induces type I and III interferons via Toll-like receptor 7 and contributes to production of NF-κB-dependent cytokines.Infection and immunity · 2014Article
- Early cytokine release in response to live Borrelia burgdorferi Sensu Lato Spirochetes is largely complement independent.PloS one · 2014Article
- The Cross-Talk between Spirochetal Lipoproteins and Immunity.Frontiers in immunology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We investigated the mechanisms that lead to the production of proinflammatory mediators by human monocytes when these cells are exposed in vitro to live Borrelia burgdorferi spirochetes. We first focused on myeloid differentiation primary response protein 88 (MyD88), an adapter molecule that is essential in the Toll-like receptor (TLR) pathway. Real-time PCR, flow cytometry, and confocal microscopy experiments revealed that MyD88 was maximally expressed in THP-1 cells after 24-h stimulation of these cells with live B. burgdorferi. Silencing of the MYD88 gene by using small interfering RNA resulted in 24%, 35%, and 84% down-modulation of the production of tumor necrosis factor alpha (TNF-alpha), interleukin-8 (IL-8), and IL-6, respectively, in THP-1 cells stimulated with live B. burgdorferi. Specific silencing of the TLR1, TLR2, or TLR5 gene by RNA interference further revealed that silencing of the TLR1 and TLR2 genes alone or combined, but not the TLR5 gene, caused a downregulation of IL-6, IL-8, and TNF-alpha in live B. burgdorferi-stimulated THP-1 cells. Overall, similar results were obtained for THP-1 cells stimulated with purified lipoproteins. Our results indicate that the TLR pathway mediates, at least in part, the release of inflammatory mediators in human monocytes stimulated with live B. burgdorferi spirochetes and furthermore suggest that the TLR-dependent interaction between these cells and live spirochetes is mediated by spirochetal lipoproteins but not by flagellin.
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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.