May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Molecular Signaling Pathways During Experimental Candida Albicans Keratitis
Author Affiliations & Notes
  • X. Yuan
    Ophthalmology, Baylor College of Medicine, Houston, Texas
  • B. Mitchell
    Ophthalmology, Baylor College of Medicine, Houston, Texas
  • K. Wilhelmus
    Ophthalmology, Baylor College of Medicine, Houston, Texas
  • Footnotes
    Commercial Relationships  X. Yuan, None; B. Mitchell, None; K. Wilhelmus, None.
  • Footnotes
    Support  NEI core grant EY02520
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 2475. doi:https://doi.org/
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      X. Yuan, B. Mitchell, K. Wilhelmus; Molecular Signaling Pathways During Experimental Candida Albicans Keratitis. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2475. doi: https://doi.org/.

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

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Abstract

Purpose: : To investigate the genetic expression profile during the early stage of posttraumatic Candida albicans keratitis in inbred mice.

Methods: : Following unilateral superficial corneal scarification of BALB/c mice, eyes were topically exposed to wild-type C. albicans (SC5314) or were mock-inoculated. After 24 hours, corneas were excised and pooled in sets of five for RNA extraction. Each experimental group was examined in triplicate by microarray using Affymetrix GeneChips® Mouse Expression Set 430, which screens for 45,101 potential murine gene transcripts. A twofold or greater difference (P < 0.05) between fungal-infected corneas compared to mock-infected controls was set as the cutoff criteria for significance. Real-time PCR was used to confirm selective gene expression patterns.

Results: : Among all tested murine genes 1,514 (3.4%) transcripts changed significantly during early infection. Inhibitory regulators of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway were significantly altered (P < .0001), including suppressors of cytokine signaling (SOCS3 and SOCS7). Genes involved in interleukin-2, interleukin-4, granulocyte-macrophage-colony stimulating factor, epidermal growth factor, and vascular endothelial growth factor pathways were significantly upregulated (P < .005). Fungal infected corneas also had increased gene expression by tenfold for tumor necrosis factor-alpha and by twofold for matrix metalloproteinase 9.

Conclusions: : Cytokine signaling within the cornea, including genetic downregulation of the JAK/STAT pathway and increased expression of genes regulating interleukins and growth factors, occurred during the initial pathogenesis of experimental C. albicans keratitis.

Keywords: fungal disease • keratitis • microbial pathogenesis: experimental studies 
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