April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Serratia Marcescens Keratitis Is Regulated By TLR4 And TLR5 And Is Dependent On MyD88 And IL-1R1
Author Affiliations & Notes
  • Rui Zhang
    School of Medicine,
    Case Western Reserve University, Cleveland, Ohio
  • Rong Zhou
    Case Western Reserve University, Cleveland, Ohio
  • Yan Sun
    Ophthalmology and Visual Sciences,
    Case Western Reserve University, Cleveland, Ohio
  • Sean Platt
    Case Western Reserve University, Cleveland, Ohio
  • Loretta Szczotka-Flynn
    Case Western Reserve University, Cleveland, Ohio
  • Eric Pearlman
    Ophthalmology and Visual Sciences,
    Case Western Reserve University, Cleveland, Ohio
  • Footnotes
    Commercial Relationships  Rui Zhang, None; Rong Zhou, None; Yan Sun, None; Sean Platt, None; Loretta Szczotka-Flynn, None; Eric Pearlman, None
  • Footnotes
    Support  NIH Grant R01 EY14362, P30 EY11373, Research to Prevent Blindness Foundation and the Ohio Lions Eye Research Foundation.
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5812. doi:
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      Rui Zhang, Rong Zhou, Yan Sun, Sean Platt, Loretta Szczotka-Flynn, Eric Pearlman; Serratia Marcescens Keratitis Is Regulated By TLR4 And TLR5 And Is Dependent On MyD88 And IL-1R1. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5812.

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

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Abstract

Purpose: : Serratia marcescens is frequently isolated from contact lenses and lens cases, and is associated with contact lens related acute red eye (CLARE). In the current study, we used a murine model of S. marcescens to examine the role of TLRs in corneal inflammation.

Methods: : The central corneal epithelium was abraded, and 1 x 10^7 S. marcescens was added. Corneal thickness and haze were examined using the ConfoScan3 microscope system, neutrophil infiltration was enumerated after immunohistochemistry, and viable bacteria were quantified by CFU. Bone marrow macrophages were stimulated with tobramycin-killed S. marcescens, and cytokine production in supernatants was measured by ELISA.

Results: : ATCC and clinical strains of S. marcescens induced time and dose dependent neutrophil recruitment to the corneal stroma and increased corneal haze and thickness in C57BL/6 mice. In vivo, these parameters were significantly lower in MyD88-/- TLR4/5-/- IL-1R-/- mice, but not in MD-2-/-, , TLR5-/-, TIRAP -/-, or TRIF-/- mice. Similarly, killed S. marcescens induced TNF-α, CXCL1 and CXCL2 production C57BL/6 macrophages in a dose dependent manner. Cytokine production was significantly lower in MyD88-/-. TLR4/5-/-, IL-1R-/-, and also in MD-2-/-, TIRAP-/- and TRIF-/- macrophages.

Conclusions: : S. marcescens - induced corneal inflammation is activated by TLR4/MD-2/MyD88 and TRIF, and by the TLR5MyD88 and IL-1R1/MyD88 - dependent pathways. These findings indicate potential therapeutic targets for S. marcescens - induced CLARE.

Keywords: cornea: basic science • keratitis • inflammation 
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