Journal
PLOS PATHOGENS
Volume 9, Issue 8, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1003575
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Funding
- National Institutes of Health (NIH), USA [N01-AI-30041]
- Canadian Institutes of Health Research (CIHR)
- Cystic Fibrosis Canada
- Chercheur-Clinicien award from the Fonds de Recherche en Sante du Quebec (FRSQ)
- grant AntiFun from the ERANet Pathogenomic program
- European Community [HEALTH-F2-2010-260338 -ALLFUN]
- Agence Nationale de la Recherche [ANR-06-EMPB-011-01]
- [R01AI073829]
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Aspergillus fumigatus is the most common cause of invasive mold disease in humans. The mechanisms underlying the adherence of this mold to host cells and macromolecules have remained elusive. Using mutants with different adhesive properties and comparative transcriptomics, we discovered that the gene uge3, encoding a fungal epimerase, is required for adherence through mediating the synthesis of galactosaminogalactan. Galactosaminogalactan functions as the dominant adhesin of A. fumigatus and mediates adherence to plastic, fibronectin, and epithelial cells. In addition, galactosaminogalactan suppresses host inflammatory responses in vitro and in vivo, in part through masking cell wall beta-glucans from recognition by dectin-1. Finally, galactosaminogalactan is essential for full virulence in two murine models of invasive aspergillosis. Collectively these data establish a role for galactosaminogalactan as a pivotal bifunctional virulence factor in the pathogenesis of invasive aspergillosis.
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