Sporothrix schenckii yeasts induce ERK pathway activation and secretion of IL-6 and TNF-α in rat mast cells, but no degranulation

Med Mycol. 2014 Nov;52(8):862-8. doi: 10.1093/mmy/myu055. Epub 2014 Sep 27.

Abstract

Sporothrix schenckii is a dimorphic fungus that causes sporotrichosis, a subcutaneous mycosis found throughout the world in humans and other mammals. After contact with conidia, transition to the yeast stage is required for establishment of infection. Mast cells are one of the first components of the immune system to make contact with invading pathogens. They release potent mediators that are decisive in initiating and directing the course of immune and inflammatory responses in the host. It remains unknown whether or not yeast cells of S. schenckii activate mast cells. Our aim in this study was to evaluate the in vitro response of mast cells to S. schenckii yeasts cells. Mast cells became activated after interaction with the yeasts, although exocytosis of preformed mediators was not stimulated. Sporothrix schenckii yeasts induced the release of early response cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6 and activation of the extracellular signal-regulated kinase (ERK) signaling pathway in mast cells. As TNF-α and IL-6 are considered crucial mediators in the defense of the host against fungal disease, the release of both mediators from mast cells may contribute to the overall response of the host immune system during S. schenckii infection.

Keywords: MAPK; Sporothrix schenckii; cytokines; mast cell; yeast.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Interleukin-6 / metabolism*
  • MAP Kinase Signaling System / immunology*
  • Male
  • Mast Cells / immunology
  • Mast Cells / metabolism*
  • Rats
  • Rats, Wistar
  • Sporothrix / immunology*
  • Sporotrichosis / microbiology
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Extracellular Signal-Regulated MAP Kinases