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High glucose may decrease the innate immune through TLRs in cornea epithelium

Hailong Ni1, Xiaoran Yan, Zhenyun Lin

  • 1Eye Center, Affiliated Second Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Molecular Vision
|January 6, 2012
PubMed
Abstract

Insights

High glucose inhibits innate immune responses in human cornea epithelial cells by downregulating toll-like receptor (TLR)2 and TLR4 expression. This finding suggests a novel mechanism for high glucose-induced immune modulation in the cornea.

Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • The innate immune system protects the cornea from pathogens.
  • Toll-like receptors (TLRs) are key components of innate immunity.
  • The effect of high glucose on corneal innate immunity is not fully understood.

Purpose of the Study:

  • To investigate the inhibitory effect of high glucose on innate immunity in cultured human cornea epithelial cells (HCEC).
  • To determine if high glucose affects HCEC by modulating toll-like receptor (TLR)2 and TLR4.

Main Methods:

  • HCEC were cultured and exposed to normal or high glucose concentrations.
  • Messenger RNA (mRNA) and protein expression of TLR2 and TLR4 were analyzed using real-time PCR, immunofluorescence, and western blot.
  • Interleukin-6 (IL-6) and IL-8 release was measured via ELISA, with and without TLR2/TLR4 blocking antibodies.

Main Results:

  • High glucose significantly inhibited mRNA and protein expression of TLR2 and TLR4 in HCEC.
  • High glucose reduced the release of IL-6 and IL-8.
  • Blocking TLR2 and TLR4 partially reversed the inhibitory effects of high glucose on cytokine release.

Conclusions:

  • High glucose concentrations can suppress the innate immune response in cornea epithelial cells.
  • This suppression appears to be mediated, at least in part, through the downregulation of TLR2 and TLR4.

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