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

Autor(es)

Jellmayer, Juliana Aparecida ; Ferreira, Lucas Souza ; Manente, Francine Alessandra ; Goncalves, Amanda Costa ; Polesi, Marisa Campos ; Batista-Duharte, Alexander ; Carlos, Iracilda Zeppone

• Tipo de documento: Artigo Científico
• Fonte: Microbial Pathogenesis; v. 110, p. 78-84, SEP 2017.
• Citações Web of Science: 11

Resumo

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)

• Processo FAPESP: 12/24187-0 - Resposta Th17 e apoptose na evolução da infecção induzida por Sporothrix schenckii
• Beneficiário: Iracilda Zeppone Carlos
• Modalidade de apoio: Auxílio à Pesquisa - Regular