ArticleInfection and immunity2011
Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Cutaneous Lyme borreliosis: Guideline of the German Dermatology Society.German medical science : GMS e-journal · 2025Guideline
- Cutaneous Lyme borreliosis: Guideline of the German Dermatology Society.German medical science : GMS e-journal · 2017Guideline
- Characterizing the impact of intracutaneous dissemination on host responses duringFrontiers in immunology · 2026Article
- Aspects of the Immunopathogenesis of Lyme Arthritis.Microorganisms · 2025Review
- Cerebrospinal fluid protein profiling of inflammatory and neurobiological markers in Lyme neuroborreliosis.Scientific reports · 2025Article
- Borrelia burgdorferi initiates early transcriptional re-programming in macrophages that supports long-term suppression of inflammation.PLoS pathogens · 2023Article
- Isocitrate binds to the itaconic acid-responsive LysR-type transcriptional regulator RipR in Salmonella pathogenesis.The Journal of biological chemistry · 2022Article
- GM-CSF suppresses antioxidant signaling and drives IL-1β secretion through NRF2 downregulation.EMBO reports · 2022Article
- Subversion of the immune response of human pathogenic spirochetes.Journal of clinical laboratory analysis · 2022Review
- Mitochondrial ACOD1/IRG1 in infection and sterile inflammation.Journal of intensive medicine · 2022Review
- Immune-responsive gene 1/itaconate activates nuclear factor erythroid 2-related factor 2 in microglia to protect against spinal cord injury in mice.Cell death & disease · 2022Article
- Irg1/itaconate metabolic pathway is a crucial determinant of dendritic cells immune-priming function and contributes to resolute allergen-induced airway inflammation.Mucosal immunology · 2022Article
- ACOD1 in immunometabolism and disease.Cellular & molecular immunology · 2020Review
- Host Metabolic Response in Early Lyme Disease.Journal of proteome research · 2020Article
- Challenge of Bovine Foot Skin Fibroblasts With Digital Dermatitis Treponemes Identifies Distinct Pathogenic Mechanisms.Frontiers in cellular and infection microbiology · 2020Article
- Autocrine IFN-I inhibits isocitrate dehydrogenase in the TCA cycle of LPS-stimulated macrophages.The Journal of clinical investigation · 2019Article
- Recent strategies for the diagnosis of early Lyme disease.Science progress · 2018Review
- Induction of Interleukin 10 by Borrelia burgdorferi Is Regulated by the Action of CD14-Dependent p38 Mitogen-Activated Protein Kinase and cAMP-Mediated Chromatin Remodeling.Infection and immunity · 2018Article
- A multi-omic analysis reveals the regulatory role of CD180 during the response of macrophages to Borrelia burgdorferi.Emerging microbes & infections · 2018Article
- Leptospirosis Pathophysiology: Into the Storm of Cytokines.Frontiers in cellular and infection microbiology · 2018Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Interleukin-10 (IL-10) modulates inflammatory responses elicited in vitro and in vivo by Borrelia burgdorferi, the Lyme disease spirochete. How IL-10 modulates these inflammatory responses still remains elusive. We hypothesize that IL-10 inhibits effector functions of multiple genes induced by B. burgdorferi in macrophages to control concomitantly elicited inflammation. Because macrophages are essential in the initiation of inflammation, we used mouse J774 macrophages and live B. burgdorferi spirochetes as the model target cell and stimulant, respectively. First, we employed transcriptome profiling to identify genes that were induced by stimulation of cells with live spirochetes and that were perturbed by addition of IL-10 to spirochete cultures. Spirochetes significantly induced upregulation of 347 genes at both the 4-h and 24-h time points. IL-10 inhibited the expression levels, respectively, of 53 and 65 of the 4-h and 24-h genes, and potentiated, respectively, at 4 h and 24 h, 65 and 50 genes. Prominent among the novel identified IL-10-inhibited genes also validated by quantitative real-time PCR (qRT-PCR) were Toll-like receptor 1 (TLR1), TLR2, IRAK3, TRAF1, IRG1, PTGS2, MMP9, IFI44, IFIT1, and CD40. Proteome analysis using a multiplex enzyme-linked immunosorbent assay (ELISA) revealed the IL-10 modulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/CXCL10, MIP-1α/CCL3, granulocyte colony-stimulating factor (G-CSF)/CSF3, CXCL1, CXCL5, CCL2, CCL4, IL-6, tumor necrosis factor alpha (TNF-α), IL-1α, IL-1β, gamma interferon (IFN-γ), and IL-9. Similar results were obtained using sonicated spirochetes or lipoprotein as stimulants. Our data show that IL-10 alters effectors induced by B. burgdorferi in macrophages to control concomitantly elicited inflammatory responses. Moreover, for the first time, this study provides global insight into potential mechanisms used by IL-10 to control Lyme disease inflammation.
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