Dectin-1-dependent LC3 recruitment to phagosomes enhances fungicidal activity in macrophages. Academic Article uri icon

Overview

MeSH

  • Animals
  • CARD Signaling Adaptor Proteins
  • Candida albicans
  • Cell Line
  • Interleukin-1beta
  • Interleukin-6
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Models, Biological
  • NADPH Oxidase
  • Phosphorylation
  • Protein-Tyrosine Kinases
  • Reactive Oxygen Species
  • Signal Transduction
  • Syk Kinase
  • Tumor Necrosis Factor-alpha
  • beta-Glucans

MeSH Major

  • Fungi
  • Lectins, C-Type
  • Macrophages
  • Microtubule-Associated Proteins
  • Phagosomes

abstract

  • Autophagy has been postulated to play role in mammalian host defense against fungal pathogens, although the molecular details remain unclear. Here, we show that primary macrophages deficient in the autophagic factor LC3 demonstrate diminished fungicidal activity but increased cytokine production in response to Candida albicans stimulation. LC3 recruitment to fungal phagosomes requires activation of the fungal pattern receptor dectin-1. LC3 recruitment to the phagosome also requires Syk signaling but is independent of all activity by Toll-like receptors and does not require the presence of the adaptor protein Card9. We further demonstrate that reactive oxygen species generation by NADPH oxidase is required for LC3 recruitment to the fungal phagosome. These observations directly link LC3 to the inflammatory pathway against C. albicans in macrophages. © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

publication date

  • December 1, 2014

has subject area

  • Animals
  • CARD Signaling Adaptor Proteins
  • Candida albicans
  • Cell Line
  • Fungi
  • Interleukin-1beta
  • Interleukin-6
  • Intracellular Signaling Peptides and Proteins
  • Lectins, C-Type
  • Macrophages
  • Mice
  • Microtubule-Associated Proteins
  • Models, Biological
  • NADPH Oxidase
  • Phagosomes
  • Phosphorylation
  • Protein-Tyrosine Kinases
  • Reactive Oxygen Species
  • Signal Transduction
  • Syk Kinase
  • Tumor Necrosis Factor-alpha
  • beta-Glucans

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC4271056

Digital Object Identifier (DOI)

  • 10.1093/infdis/jiu290

PubMed ID

  • 24842831

Additional Document Info

start page

  • 1844

end page

  • 1854

volume

  • 210

number

  • 11