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Innate immune responses in Lyme borreliosis: enhanced tumour necrosis factor-α and interleukin-12 in asymptomatic individuals in response to live spirochetes

Sjowall J, Carlsson A, Vaarala O +4 more2005Clinical & Experimental ImmunologyJournal Article
10.1111/j.1365-2249.2005.02820.xPubMedFree full text
Immune/InnateNeurological
Lyme & Co-Infections

Abstract

SummaryInnate immunity is important for early defence against borrelia spirochetes and should play a role in the clinical outcome of the infection. In order to study early cytokine responses, in vitro differentiated dendritic cells (DCs) and whole blood cells from 21 patients with different clinical outcomes of Lyme neuroborreliosis were stimulated with live borrelia spirochetes. The borrelia-induced secretion of interleukin (IL)-4, IL-10, IL-12p70, interferon (IFN)-γ and tumour necrosis factor (TNF)-α in DCs and IL-1β, IL-6, IL-8, IL-10, IL-12p70, TNF-α, regulated upon activation normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, MIP-1β and eotaxin in whole blood cells was measured by enzyme-linked immunospot (ELISPOT) and multiplex arrays, respectively. We found increased numbers of TNF-α-secreting DCs (P = 0·018) in asymptomatic seropositive individuals compared to patients with subacute neuroborreliosis and seronegative controls. Asymptomatic individuals were also found to have elevated levels of IL-12p70 (P = 0·031) in whole blood cell supernatants compared to seronegative controls. These results are in line with previous experiments using cells of the adaptive immune response, indicating that strong T helper type 1 (Th1) proinflammatory responses might be associated with a successful resolution of Lyme disease.

Key Biomarkers

EotaxinIFN-γIL-10IL-12p70IL-1βIL-4IL-6IL-8MCP-1MIP-1αMIP-1βRANTESTNF-α

Symptom Clusters

Asymptomatic seropositiveSubacute neuroborreliosis

Cited By (3)

  • Propensity to excessive proinflammatory response in chronic Lyme BorreliosisApmis · 2007
  • Interleukin-10 Anti-Inflammatory Response toBorrelia burgdorferi, the Agent of Lyme Disease: a Possible Role for Suppressors of Cytokine Signaling 1 and 3Infection and Immunity · 2006
  • Complement activation in Lyme neuroborreliosis — Increased levels of C1q and C3a in cerebrospinal fluid indicate complement activation in the CNSJournal of Neuroimmunology · 2007

References (5)

  • Lipoproteins of Borrelia burgdorferi and Treponema pallidum activate cachectin/tumor necrosis factor synthesis. Analysis using a CAT reporter constructThe Journal of Immunology · 1991
  • An epidemiologic study of Lyme disease in southern SwedenNew England Journal of Medicine · 1995
  • The clinical evolution of Lyme arthritisAnnals of Internal Medicine · 1987

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