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High serum CXCL10 in Rickettsia conorii infection is endothelial cell mediated subsequent to whole blood activation.
Oslo University Hospital Rikshospitalet, Norway.
Hospital San Pedro-Center of Biomedical Research from La Rioja (CIBIR), Spain.
Oslo University Hospital Rikshospitalet, Norway ; University of Oslo, Norway.
Research Laboratory Nordland Hospital, Norway.
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2016 (English)In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 83, p. 269-274Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The pathophysiological hallmark of Rickettsia conorii (R. conorii) infection comprises infection of endothelial cells with perivascular infiltration of T-cells and macrophages. Although interferon (IFN)-γ-induced protein 10 (IP-10)/CXCL10 is induced during vascular inflammation, data on CXCL10 in R. conorii infection is scarce.

METHODS: Serum CXCL10 was analyzed in two cohorts of southern European patients with R. conorii infection using multiplex cytokine assays. The mechanism of R. conorii-induced CXCL10 release was examined ex vivo using human whole blood interacting with endothelial cells.

RESULTS: (i) At admission, R. conorii infected patients had excessively increased CXCL10 levels, similar in the Italian (n=32, ∼56-fold increase vs controls) and the Spanish cohort (n=38, ∼68-fold increase vs controls), followed by a marked decrease after recovery. The massive CXCL10 increase was selective since it was not accompanied with similar changes in other cytokines. (ii) Heat-inactivated R. conorii induced a marked CXCL10 increase when whole blood and endothelial cells were co-cultured. Even plasma obtained from R. conorii-exposed whole blood induced a marked CXCL10 release from endothelial cells, comparable to the levels found in serum of R. conorii-infected patients. Bacteria alone did not induce CXCL10 production in endothelial cells, macrophages or smooth muscle cells.

CONCLUSIONS: We show a massive and selective serum CXCL10 response in R. conorii-infected patients, likely reflecting release from infected endothelial cells characterized by infiltrating T cells and monocytes. The CXCL10 response could contribute to T-cell infiltration within the infected organ, but the pathologic consequences of CXCL10 in clinical R. conorii infection remain to be defined.

Place, publisher, year, edition, pages
2016. Vol. 83, p. 269-274
National Category
Immunology in the medical area
Research subject
Biomedical Sciences, Immunology
Identifiers
URN: urn:nbn:se:lnu:diva-60954DOI: 10.1016/j.cyto.2016.05.006ISI: 000377228300036PubMedID: 27180202OAI: oai:DiVA.org:lnu-60954DiVA, id: diva2:1077195
Available from: 2017-02-26 Created: 2017-02-26 Last updated: 2018-01-13Bibliographically approved

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Nilsson, Per H.

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