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Propensity to excessive proinflammatory response in chronic Lyme Borreliosis

Kisland KE, Prukk T, Kisand K +3 more2007ApmisJournal Article
10.1111/j.1600-0463.2007.apm_538.xPubMed
Immune/InnateMusculoskeletalNeurological
Lyme & Co-Infections

Abstract

The clinical course of Lyme borreliosis is extremely variable. However, all the clinical manifestations, acute or chronic, are characterized by strong inflammation. Borrelia burgdorferi can induce the production of several proinflammatory and anti‐inflammatory cytokines. The aim of our study was to find out whether the balance between inflammatory and regulatory mechanisms is important in determining the course of Lyme borreliosis. 13 patients with early Lyme borreliosis, 8 patients with chronic Lyme disease with neurological or joint manifestations, and 15 age‐ and sex‐matched healthy controls were studied. Chronic forms of Lyme borreliosis were characterized by stronger TNF‐α response by monocytes to lipopolysaccharide as well as to borrelia antigen compared to early Lyme borreliosis and the healthy state. The percentage of IL‐10‐secreting monocytes in response to borrelia lysate was lower in the Lyme borreliosis patients than in healthy controls. The percentage of CD4+ CTLA‐4+ regulatory T cells showed the highest values in early Lyme borreliosis. We conclude that chronic forms of Lyme borreliosis can evolve due to an aberrant innate proinflammatory response.

Key Biomarkers

CD4+ CTLA-4+ regulatory T cellsIL-10Monocyte proinflammatory responseTNF-α

Symptom Clusters

Chronic neurological manifestationsJoint manifestationsStrong inflammation

References (5)

  • Innate immune responses in Lyme borreliosis: enhanced tumour necrosis factor-α and interleukin-12 in asymptomatic individuals in response to live spirochetesClinical & Experimental Immunology · 2005
  • Dual Role of Interleukin-10 in Murine Lyme Disease: Regulation of Arthritis Severity and Host DefenseInfection and Immunity · 1999
  • Association of CD4+CD25+T Cells with Prevention of Severe Destructive Arthritis inBorrelia burgdorferi-Vaccinated and Challenged Gamma Interferon-Deficient Mice Treated with Anti-Interleukin-17 AntibodyClinical and Vaccine Immunology · 2004
  • Induction of Pro- and Anti-Inflammatory Cytokines byBorrelia burgdorferiLipoproteins in Monocytes Is Mediated by CD14Infection and Immunity · 1999
  • Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient miceNature Medicine · 2002

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