April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
An Essential Role for Dectin 1 in the Pathogenesis of Aspergillus fumigatus Keratitis
Author Affiliations & Notes
  • S. M. Leal, Jr.
    Case Western Reserve University, Cleveland, Ohio
  • Y. Sun
    Case Western Reserve University, Cleveland, Ohio
  • E. Pearlman
    Case Western Reserve University, Cleveland, Ohio
  • Footnotes
    Commercial Relationships  S.M. Leal, Jr., None; Y. Sun, None; E. Pearlman, None.
  • Footnotes
    Support  NIH Grant 1R01EY018612-01; Research to Prevent Blindness Grant TRN108083
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 2400. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      S. M. Leal, Jr., Y. Sun, E. Pearlman; An Essential Role for Dectin 1 in the Pathogenesis of Aspergillus fumigatus Keratitis. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2400.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements

Purpose: : Dectin 1 is a C-type lectin receptor primarily expressed on macrophages and dendritic cells. Its ligand is the ubiquitous fungal cell wall constituent ß (1,3) glucan. Surface expression of ß-glucan depends on the stage of fungal development. For the filamentous fungal pathogen Aspergillus fumigatus , ß-glucan surface exposure is absent during the highly transmissible conidial stage (spore-form), but expressed constitutively upon germination and progression through the post-germination stages (swollen conidia, germ tube, and hyphal stages) of fungal development. This observation led us to hypothesize that Dectin 1 is involved in the innate immune recognition and the subsequent inflammatory response initiated upon germination of A.fumigatus conidia in fungal keratitis (corneal infection).

Methods: : To address this hypothesis, we developed a mouse model in which 10^5 A. fumigatus conidia was injected into the corneal stroma of WT 129SvEv or Dectin 1-/- mice. The organisms were allowed to subsequently germinate, and clinical disease progression, neutrophil recruitment, & fungal viability assessed 24 Hr later.

Results: : Using this model, we identified a role for Dectin 1 in the recognition of the post-germination developmental stages of A.fumigatus, but not in response to resting conidia, which do not express ß-glucan. Clinical disease severity and neutrophilic infiltration was significantly reduced in Dectin 1-/- mice, though at the 24 Hr timepoint no difference in fungal survival was observed.

Conclusions: : These data implicate a role for Dectin 1 in the pathogenesis of Aspergillus fumigatus keratitis, and gives credence to the potential therapeutic benefit of targeting the Dectin 1 signaling pathway in an effort to minimize the inflammatory-mediated corneal pathology during Aspergillus keratitis.

Keywords: fungal disease • inflammation • cornea: basic science 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.