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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Dectin-1 expression by macrophages and related antifungal mechanisms in a murine model of Sporothrix schenckii sensu stricto systemic infection

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Author(s):
Jellmayer, Juliana Aparecida ; Ferreira, Lucas Souza ; Manente, Francine Alessandra ; Goncalves, Amanda Costa ; Polesi, Marisa Campos ; Batista-Duharte, Alexander ; Carlos, Iracilda Zeppone
Total Authors: 7
Document type: Journal article
Source: Microbial Pathogenesis; v. 110, p. 78-84, SEP 2017.
Web of Science Citations: 11
Abstract

The available information about the role of Dectin-1 in sporotrichosis is scarce. Hence, we aimed to assess Dectin-1 expression by macrophages and the activation of some related antifungal mechanisms during the Sporothrix schenckii sensu stricto infection as a first attempt to elucidate the role of this receptor in sporotrichosis. Balb/c mice were intraperitoneally infected with S. schenckii sensu stricto yeast ATCC 16345 and euthanized on days 5, 10 and 15 post-infection, when the following parameters were evaluated: fungal burden in spleen, Dectin-1 expression and nitric oxide (NO) production by peritoneal macrophages, as well as IL-1 beta, TNF-alpha: and IL-10 ex vivo secretion by these same cells. Peritoneal macrophages were ex vivo challenged with either the alkali-insoluble fraction (Fl) extracted from the S. schenckii cell wall, a commercially available purified beta-1,3-glucan or whole heat-killed S. schenckii yeasts (HKss). Additionally, a Dectin-1 antibody-mediated blockade assay was performed on day 10 post infection to assess the participation of this receptor in cytokine secretion. Our results showed that Dectin-1 expression by peritoneal macrophages was augmented on days 10 and 15 post-infection alongside elevated NO production and ex vivo secretion of IL-10, TNF-alpha and IL-1 beta. The antibody mediated blockade of Dectin-1 inhibited cytokine production in both infected and non-infected mice, mainly after beta-1,3-glucan stimulation. Our results suggest a role for Dectin-1 in triggering the immune response during S. schenckii infection. (C) 2017 Elsevier Ltd. All rights reserved. (AU)

FAPESP's process: 12/24187-0 - Th17 response and apoptosis in the evolution of Sporothrix schenckii-induced infection
Grantee:Iracilda Zeppone Carlos
Support Opportunities: Regular Research Grants