Purchase this article with an account.
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.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
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.
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.
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.
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.
This PDF is available to Subscribers Only