May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Liposomal C6-Ceramide Inhibits Toll Like Receptor (tlr) - Induced Cxc Chemokine Production by Corneal Epithelial Cells and Tlr - Mediated Corneal Inflammation
Author Affiliations & Notes
  • Y. Sun
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio
  • T. Fox
    Pharmacology, Penn State, Hershey, Pennsylvania
  • M. Kester
    Pharmacology, Penn State, Hershey, Pennsylvania
  • E. Pearlman
    Ophthalmology, Case Western Reserve University, Cleveland, Ohio
  • Footnotes
    Commercial Relationships Y. Sun, Bausch and Lomb, Inc., F; T. Fox, None; M. Kester, None; E. Pearlman, Bausch and Lomb, Inc., F.
  • Footnotes
    Support EY14362, EY11373, EY015800 HIGHWIRE EXLINK_ID="48:5:5987:1" VALUE="EY015800" TYPEGUESS="GEN" /HIGHWIRE , Bausch and Lomb, Inc., The Research to Prevent Blindness Foundation, Ohio Lions Eye Research Foundation.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5987. doi:
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    • Get Citation

      Y. Sun, T. Fox, M. Kester, E. Pearlman; Liposomal C6-Ceramide Inhibits Toll Like Receptor (tlr) - Induced Cxc Chemokine Production by Corneal Epithelial Cells and Tlr - Mediated Corneal Inflammation. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5987.

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

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Abstract

Purpose:: Activation of Toll-like receptors (TLR) in the corneal epithelium induces an inflammatory response characterized by neutrophil infiltration and loss of corneal clarity. The purpose of the current study was to determine the effect of liposomal C6-ceramide (Lip-C6) on TLR - induced keratitis.

Methods:: Liposomes were prepared containing 30 molar C6-ceramide, and control (ghost) liposomes were made in the absence of ceramide. Human corneal epithelial cells were treated with Lip-C6 or ghost liposomes prior to stimulation with inactivated Staphylococcus aureus (TLR2 agonist), and CXC chemokine production was measured by ELISA. For corneal inflammation, C57BL/6 corneas were abraded and treated with Lip-C6 or ghost liposomes prior to activation with S. aureus or LPS, and neutrophil infiltration and corneal haze were measured.

Results:: Lip-C6, but not control liposomes, inhibited production of CXCL1, CXCL5 and CXCL8. Furthermore, topical application of Lip-C6 to mouse corneas significantly inhibited S. aureus - and LPS - induced corneal inflammation as measured by neutrophil infiltration to the corneal stroma and development of corneal haze. Despite the reported activity for ceramides, Lip-C6 did not induce apoptosis of corneal epithelial cells in vitro or in vivo, nor did it inhibit corneal wound healing.

Conclusions:: Together, these findings demonstrate a novel anti-inflammatory, non-toxic, therapeutic role for liposomally-delivered short-chain C6-ceramide in a model of ocular inflammation and resultant visual impairment.

Keywords: inflammation • keratitis • Staphylococcus 
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