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Article Dans Une Revue Cytokine Année : 2016

High serum CXCL10 in Rickettsia conorii infection is endothelial cell ă mediated subsequent to whole blood activation

Kari Otterdal
  • Fonction : Auteur
Aranzazu Portillo
  • Fonction : Auteur
Elisabeth Astrup
  • Fonction : Auteur
Judith Ă Ludviksen
  • Fonction : Auteur
Giovanni Davi
  • Fonction : Auteur
Sverre Holm
  • Fonction : Auteur
Ă Francesca Santilli
  • Fonction : Auteur
Giustina Vitale
  • Fonction : Auteur
Juan P. Olano
  • Fonction : Auteur
Camilla Ă Schjalm
  • Fonction : Auteur
Bente Halvorsen
  • Fonction : Auteur
Jose A. Oteo
  • Fonction : Auteur
Tom Ă Eirik Mollnes
  • Fonction : Auteur
Pal Aukrust
  • Fonction : Auteur
Per H. Nilsson
  • Fonction : Auteur

Résumé

Background: The pathophysiological hallmark of Rickettsia conorii (R. ă conorii) infection comprises infection of endothelial cells with ă perivascular infiltration of T-cells and macrophages. Although ă interferon (IFN)-gamma-induced protein 10 (IP-10)/CXCL10 is induced ă during vascular inflammation, data on CXCL10 in R. conorii infection is ă scarce. ă Methods: Serum CXCL10 was analyzed in two cohorts of southern European ă patients with R. conorii infection using multiplex cytokine assays. The ă mechanism of R. conorii-induced CXCL10 release was examined ex vivo ă using human whole blood interacting with endothelial cells. ă Results: (i) At admission, R. conorii infected patients had excessively ă increased CXCL10 levels, similar in the Italian (n = 32, similar to ă 56-fold increase vs controls) and the Spanish cohort (n = 38, 68-fold ă increase vs controls), followed by a marked decrease after recovery. The ă massive CXCL10 increase was selective since it was not accompanied with ă similar changes in other cytokines. (ii) Heat-inactivated R. conorii ă induced a marked CXCL10 increase when whole blood and endothelial cells ă were co-cultured. Even plasma obtained from R. conorii-exposed whole ă blood induced a marked CXCL10 release from endothelial cells, comparable ă to the levels found in serum of R. conorii-infected patients. Bacteria ă alone did not induce CXCL10 production in endothelial cells, macrophages ă or smooth muscle cells. ă Conclusions: We show a massive and selective serum CXCL10 response in R. ă conorii-infected patients, likely reflecting release from infected ă endothelial cells characterized by infiltrating T cells and monocytes. ă The CXCL10 response could contribute to T-cell infiltration within the ă infected organ, but the pathologic consequences of CXCL10 in clinical R. ă conorii infection remain to be defined. (C) 2016 Elsevier Ltd. All ă rights reserved.
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Dates et versions

hal-01465136 , version 1 (10-02-2017)

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Kari Otterdal, Aranzazu Portillo, Elisabeth Astrup, Judith Ă Ludviksen, Giovanni Davi, et al.. High serum CXCL10 in Rickettsia conorii infection is endothelial cell ă mediated subsequent to whole blood activation. Cytokine, 2016, 83, pp.269-274. ⟨10.1016/j.cyto.2016.05.006⟩. ⟨hal-01465136⟩

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