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A complex interaction between Rickettsia conorii and Dickkopf-1--potential role in immune evasion mechanisms in

Elisabeth Astrup1, Tove Lekva, Giovanni Davì

  • 1Institute of Clinical Medicine, Akershus University Hospital, Lørenskog, Norway. Elisabeth.Astrup.Strand@rr-research.no

Plos One
|October 3, 2012
PubMed

Insights

Dickkopf-1 (DKK-1) levels rise during Rickettsia conorii infections, indicating its role in inflammation. Down-regulation of DKK-1 by R. conorii may be a mechanism for immune evasion.

Area of Science:

  • Vascular Biology
  • Immunology
  • Microbiology

Background:

  • Spotted fever group rickettsioses are characterized by vascular inflammation.
  • Wingless (Wnt) signaling pathways are increasingly recognized for their roles in inflammation and vascular biology.
  • Dickkopf-1 (DKK-1), a Wnt signaling modulator, is investigated for its potential role in rickettsial infection pathogenesis.

Purpose of the Study:

  • To investigate the role of Dickkopf-1 (DKK-1) in the pathogenesis of Rickettsia conorii infection.
  • To explore the relationship between DKK-1 levels and inflammation in patients with R. conorii infection.
  • To elucidate the in vitro effects of R. conorii on endothelial DKK-1 production and the subsequent impact on inflammation and thrombosis.

Main Methods:

  • Quantified DKK-1 concentrations in patients with R. conorii infection and healthy controls.
  • Conducted in vitro experiments using human umbilical vein endothelial cells (HUVECs) exposed to heat-inactivated R. conorii.
  • Utilized gene silencing techniques to assess the functional impact of DKK-1 on endothelial cell responses.

Main Results:

  • DKK-1 levels were not significantly different at baseline but rose significantly during R. conorii infection.
  • Heat-inactivated R. conorii down-regulated endothelial DKK-1 release while enhancing IL-6 and IL-8 production.
  • Silencing DKK-1 attenuated R. conorii-induced release of IL-6, IL-8, and GRO-α, and modulated tissue factor and thrombomodulin expression.

Conclusions:

  • R. conorii infection leads to increased DKK-1 levels in patients.
  • R. conorii actively down-regulates endothelial DKK-1, potentially contributing to inflammation.
  • DKK-1 plays a role in mediating R. conorii-induced inflammation and pro-thrombotic effects in endothelial cells, suggesting a novel immune evasion mechanism.

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