ArticlePLoS pathogens2014
MicroRNA-146a provides feedback regulation of lyme arthritis but not carditis during infection with Borrelia burgdorferi.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Noncoding RNAs in skeletal development and disorders.Biological research · 2024Review
- Effect ofMicroorganisms · 2023Article
- Endogenous Linear Plasmids lp28-4 and lp25 Are Required for Infectivity and Restriction Protection in the Lyme Disease Spirochete Borrelia mayonii.Infection and immunity · 2023Article
- Effects of Regulatory T Cell Depletion in BALB/c Mice Infected with Low Doses ofPathogens (Basel, Switzerland) · 2023Article
- Mechanisms and application strategies of miRNA‑146a regulating inflammation and fibrosis at molecular and cellular levels (Review).International journal of molecular medicine · 2023Review
- Borrelia burgdorferi-mediated induction of miR146a-5p fine tunes the inflammatory response in human dermal fibroblasts.PloS one · 2023Article
- Lyme disease and the pursuit of a clinical cure.Frontiers in medicine · 2023Review
- MicroRNAs as Regulators of Phagocytosis.Cells · 2022Review
- Lyme arthritis: linking infection, inflammation and autoimmunity.Nature reviews. Rheumatology · 2021Review
- Lipopolysaccharide-Induced Exosomal miR-146a Is Involved in Altered Expression of Alzheimer's Risk Genes Via Suppression of TLR4 Signaling.Journal of molecular neuroscience : MN · 2021Article
- Host transcriptome response to Borrelia burgdorferi sensu lato.Ticks and tick-borne diseases · 2021Review
- A murine model of Lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system.PLoS pathogens · 2021Article
- Peripheral blood mononuclear cell microRNA profiles in syphilitic patients with serofast status.Molecular biology reports · 2020Article
- A joint effort: The interplay between the innate and the adaptive immune system in Lyme arthritis.Immunological reviews · 2020Review
- Epigenetic Changes Associated With Interleukin-10.Frontiers in immunology · 2020Review
- Biologic Markers of Antibiotic-Refractory Lyme Arthritis in Human: A Systematic Review.Infectious diseases and therapy · 2019Review
- Functional Regulation of Macrophage Phenotypes by MicroRNAs in Inflammatory Arthritis.Frontiers in immunology · 2019Review
- miR-146a regulates the crosstalk between intestinal epithelial cells, microbial components and inflammatory stimuli.Scientific reports · 2018Article
- IL-10 Deficiency Reveals a Role for TLR2-Dependent Bystander Activation of T Cells in Lyme Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Delivery of miR-146a to Ly6CTheranostics · 2018Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
MicroRNAs have been shown to be important regulators of inflammatory and immune responses and are implicated in several immune disorders including systemic lupus erythematosus and rheumatoid arthritis, but their role in Lyme borreliosis remains unknown. We performed a microarray screen for expression of miRNAs in joint tissue from three mouse strains infected with Borrelia burgdorferi. This screen identified upregulation of miR-146a, a key negative regulator of NF-κB signaling, in all three strains, suggesting it plays an important role in the in vivo response to B. burgdorferi. Infection of B6 miR-146a-/- mice with B. burgdorferi revealed a critical nonredundant role of miR-146a in modulating Lyme arthritis without compromising host immune response or heart inflammation. The impact of miR-146a was specifically localized to the joint, and did not impact lesion development or inflammation in the heart. Furthermore, B6 miR-146a-/- mice had elevated levels of NF-κB-regulated products in joint tissue and serum late in infection. Flow cytometry analysis of various lineages isolated from infected joint tissue of mice showed that myeloid cell infiltration was significantly greater in B6 miR-146a-/- mice, compared to B6, during B. burgdorferi infection. Using bone marrow-derived macrophages, we found that TRAF6, a known target of miR-146a involved in NF-κB activation, was dysregulated in resting and B. burgdorferi-stimulated B6 miR-146a-/- macrophages, and corresponded to elevated IL-1β, IL-6 and CXCL1 production. This dysregulated protein production was also observed in macrophages treated with IL-10 prior to B. burgdorferi stimulation. Peritoneal macrophages from B6 miR-146a-/- mice also showed enhanced phagocytosis of B. burgdorferi. Together, these data show that miR-146a-mediated regulation of TRAF6 and NF-κB, and downstream targets such as IL-1β, IL-6 and CXCL1, are critical for modulation of Lyme arthritis during chronic infection with B. burgdorferi.
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