Literature DB >> 22246581

Association of a Toll-like receptor 1 polymorphism with heightened Th1 inflammatory responses and antibiotic-refractory Lyme arthritis.

Klemen Strle1, Junghee J Shin, Lisa J Glickstein, Allen C Steere.   

Abstract

OBJECTIVE: Single-nucleotide polymorphisms (SNPs) that alter immune function, inflammatory responses, and disease susceptibility have been identified in several genes encoding Toll-like receptors (TLRs). The TLR SNPs with the best evidence of an effect on immune function are those in TLR1 (1805GG), TLR2 (2258GA), and TLR5 (1174CT). This study was undertaken to assess the frequency and functional outcomes of these polymorphisms in patients with Lyme disease.
METHODS: SNP frequencies and functional outcomes were assessed in 248 patients with Lyme disease. Cytokine and chemokine levels were determined using multiplex assays in the serum of patients with erythema migrans (EM), joint fluid of patients with Lyme arthritis, and supernatants of Borrelia burgdorferi-stimulated peripheral blood mononuclear cells (PBMCs) from patients with Lyme arthritis.
RESULTS: The frequency of the TLR1-1805GG polymorphism was greater in patients with antibiotic-refractory arthritis compared with patients with EM or those with antibiotic-responsive arthritis. Early in the illness, patients with EM carrying 1805GG, primarily those infected with B burgdorferi 16S-23S ribosomal spacer RNA intergenic type 1 (RST1) strains, had higher serum levels of interferon-γ (IFNγ), CXCL9, and CXCL10 and had more severe infection than EM patients carrying the 1805TG/TT polymorphism. These inflammatory responses were amplified in patients with Lyme arthritis, and the highest responses were observed in patients with 1805GG in the antibiotic-refractory group who had been infected with RST1 strains. When PBMCs from patients with Lyme arthritis were stimulated with a B burgdorferi RST1 strain, the 1805GG group had a significantly larger fold increase in the levels of IFNγ, CCL2, CXCL9, and CXCL10 compared to the 1805TG/TT group. In contrast, the TLR2 and TLR5 polymorphisms did not vary in frequency or function among the groups.
CONCLUSION: The TLR1-1805GG polymorphism in B burgdorferi RST1-infected patients was associated with stronger Th1-like inflammatory responses, an environment that may set the stage for antibiotic-refractory arthritis.
Copyright © 2012 by the American College of Rheumatology.

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Year:  2012        PMID: 22246581      PMCID: PMC3338893          DOI: 10.1002/art.34383

Source DB:  PubMed          Journal:  Arthritis Rheum        ISSN: 0004-3591


  48 in total

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Authors:  Allen C Steere; Sheryn M Angelis
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4.  Heterozygous Arg753Gln polymorphism of human TLR-2 impairs immune activation by Borrelia burgdorferi and protects from late stage Lyme disease.

Authors:  Nicolas W J Schröder; Isabel Diterich; Antje Zinke; Jana Eckert; Christian Draing; Volker von Baehr; Dieter Hassler; Susanne Priem; Katrin Hahn; Kathrin S Michelsen; Thomas Hartung; Gerd R Burmester; Ulf B Göbel; Corinna Hermann; Ralf R Schumann
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Authors:  Gary P Wormser; Raymond J Dattwyler; Eugene D Shapiro; John J Halperin; Allen C Steere; Mark S Klempner; Peter J Krause; Johan S Bakken; Franc Strle; Gerold Stanek; Linda Bockenstedt; Durland Fish; J Stephen Dumler; Robert B Nadelman
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9.  High levels of inflammatory chemokines and cytokines in joint fluid and synovial tissue throughout the course of antibiotic-refractory lyme arthritis.

Authors:  Junghee J Shin; Lisa J Glickstein; Allen C Steere
Journal:  Arthritis Rheum       Date:  2007-04

10.  Antibiotic-refractory Lyme arthritis is associated with HLA-DR molecules that bind a Borrelia burgdorferi peptide.

Authors:  Allen C Steere; William Klitz; Elise E Drouin; Ben A Falk; William W Kwok; Gerald T Nepom; Lee Ann Baxter-Lowe
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1.  Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy.

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2.  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.

Authors:  Bikash Sahay; Kathleen Bashant; Nicole L J Nelson; Rebeca L Patsey; Shiva Kumar Gadila; Rebecca Boohaker; Ashutosh Verma; Klemen Strle; Timothy J Sellati
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3.  CCL19 as a Chemokine Risk Factor for Posttreatment Lyme Disease Syndrome: a Prospective Clinical Cohort Study.

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4.  Autoimmune Arthritides, Rheumatoid Arthritis, Psoriatic Arthritis, or Peripheral Spondyloarthritis Following Lyme Disease.

Authors:  Sheila L Arvikar; Jameson T Crowley; Katherine B Sulka; Allen C Steere
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5.  Robust interferon signature and suppressed tissue repair gene expression in synovial tissue from patients with postinfectious, Borrelia burgdorferi-induced Lyme arthritis.

Authors:  Robert B Lochhead; Sheila L Arvikar; John M Aversa; Ruslan I Sadreyev; Klemen Strle; Allen C Steere
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6.  Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease.

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7.  Correlation of Lyme Disease-Associated IgG4 Autoantibodies With Synovial Pathology in Antibiotic-Refractory Lyme Arthritis.

Authors:  Katherine B Sulka; Klemen Strle; Jameson T Crowley; Robert B Lochhead; Robert Anthony; Allen C Steere
Journal:  Arthritis Rheumatol       Date:  2018-09-24       Impact factor: 10.995

8.  Interleukin-10 (IL-10) inhibits Borrelia burgdorferi-induced IL-17 production and attenuates IL-17-mediated Lyme arthritis.

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Journal:  Infect Immun       Date:  2013-09-16       Impact factor: 3.441

9.  Dysregulation of CD4+CD25(high) T cells in the synovial fluid of patients with antibiotic-refractory Lyme arthritis.

Authors:  Nalini K Vudattu; Klemen Strle; Allen C Steere; Elise E Drouin
Journal:  Arthritis Rheum       Date:  2013-06

Review 10.  Review: unraveling Lyme disease.

Authors:  Linda K Bockenstedt; Gary P Wormser
Journal:  Arthritis Rheumatol       Date:  2014-09       Impact factor: 10.995

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