Interleukin-27 Early Impacts Leishmania infantum Infection in Mice and Correlates with Active Visceral Disease in Humans

• Type: Article in International Scientific Journal
• Date: 2016

Authors

Perez Cabezas, B (Author) Other; Cecilio, P (Author) Other; Robalo, AL (Author) Other; Silvestre, R (Author) Other; Carrillo, E (Author) Other; Moreno, J (Author) Other; San Martin, JV (Author) Other; Vasconcellos, R (Author) Other; Anabela Cordeiro da Silva (Author) FFUP

Journal

Title: Frontiers In Immunology

Vol. 7

ISSN: 1664-3224

Publisher: Frontiers Media

Indexing

ISI Web of Knowledge - 12 Citations

Scopus - 12 Citations

Other information

Authenticus ID: P-00M-77Z

DOI: 10.3389/fimmu.2016.00478

Abstract (EN): The complexity of Leishmania host interactions, one of the main leishmaniasis issues, is yet to be fully understood. We detected elevated IL-27 plasma levels in European patients with active visceral disease caused by Leishmania infantum, which returned to basal levels after successful treatment, suggesting this cytokine as a probable infection mediator. We further addressed this hypothesis recurring to two classical susceptible visceral leishmaniasis mouse models. BALB/c, but not C57BU6 mice, showed increased IL-27 systemic levels after infection, which was associated with an upregulation of IL-27p28 expression by dendritic cells and higher parasite burdens. Neutralization of IL-27 in acutely infected BALB/c led to decreased parasite burdens and a transient increase in IFN-gamma(+) splenic T cells, while administration of IL-27 to C57BU6 promoted a local anti-inflammatory cytokine response at the site of infection and increased parasite loads. Overall, we show that, as in humans, BALB/c IL-27 systemic levels are infection dependently upregulated and may favor parasite installation by controlling inflammation.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 12