May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Toll Like Receptor 4 Initiates an Innate Immune Response to Lipopolysacccharide in Human Conjunctival Epithelial Cells
Author Affiliations & Notes
  • S.-H. Chung
    Ophthalmology, The Catholic University of Korea, Seoul, Republic of Korea
  • M.-N. Kweon
    Mucosal Immunology Section, International Vaccine Institute, Seoul, Republic of Korea
  • H. Lee
    Ophthalmology, Cornea Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea
  • J.-Y. Yang
    Mucosal Immunology Section, International Vaccine Institute, Seoul, Republic of Korea
  • E. Kim
    Ophthalmology, Cornea Dystrophy Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships  S. Chung, None; M. Kweon, None; H. Lee, None; J. Yang, None; E. Kim, None.
  • Footnotes
    Support  The Korea Research Foundation Grant (MOEHRD, Basic Research Promotion Fund), and The Korea Science and Engineering Foundation grant
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5147. doi:https://doi.org/
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    • Get Citation

      S.-H. Chung, M.-N. Kweon, H. Lee, J.-Y. Yang, E. Kim; Toll Like Receptor 4 Initiates an Innate Immune Response to Lipopolysacccharide in Human Conjunctival Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5147. doi: https://doi.org/.

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

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Abstract

Purpose: : Conjunctival epithelial cells serve as a first line of defense against pathogens presented to the innate immune system. The inflammatory response to Gram-negative bacteria is initiated by Toll-like receptor 4 (TLR4). The purpose of our study was to investigate whether a TLR4 ligand induces production of inflammatory cytokines in human conjunctival epithelial cells (HCECs) through nuclear factor kappa-B (NF-ΚB).

Methods: : HCECs were stimulated with various concentrations of lipopolysaccharide (LPS). HCECs were evaluated for TLR4 expression by reverse transcriptase polymerase chain reaction (RT-PCR) and flow cytometric analysis. The innate immune response was quantified by measuring expression of the inflammatory cytokines IL-6 and IL-8. Functional NF-ΚB activation was examined using a luciferase reporter assay.

Results: : Expression of TLR4-specific mRNA as well as its corresponding protein was observed both intracellularly and on the cell surface of HCECs. Incubation of HCECs with LPS led to activation of the NF-ΚB transcription factor and secretion of IL-6 and IL-8 in a dose dependent manner. Blockade of TLR4 and TRAF6 activity abolished induction of the inflammatory response to LPS in HCECs. LPS did not induce the expression of TLR4 in HCECs.

Conclusions: : Our results demonstrated that surface expression of TLR4 in human conjunctival epithelial cells was able to elicit a TLR4-mediated innate immune response and contribute to an inflammatory environment on the ocular surface.

Keywords: conjunctiva • inflammation • immunomodulation/immunoregulation 
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