September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
The role of IL-1R and MyD88 in a murine model of experimental dry eye
Author Affiliations & Notes
  • Justin A Courson
    Ocular Surface Institute, University of Houston, Houston, Texas, United States
  • Carolina Lema
    Ocular Surface Institute, University of Houston, Houston, Texas, United States
  • Betty Zhang
    Ocular Surface Institute, University of Houston, Houston, Texas, United States
  • Rachel L Redfern
    Ocular Surface Institute, University of Houston, Houston, Texas, United States
  • Footnotes
    Commercial Relationships   Justin Courson, None; Carolina Lema, None; Betty Zhang, None; Rachel Redfern, None
  • Footnotes
    Support  NIH NEI R01 EY023628
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 405. doi:
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    • Get Citation

      Justin A Courson, Carolina Lema, Betty Zhang, Rachel L Redfern; The role of IL-1R and MyD88 in a murine model of experimental dry eye. Invest. Ophthalmol. Vis. Sci. 2016;57(12):405.

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

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Abstract

Purpose : Previously we have shown that experimental dry eye (EDE) increases toll-like receptor (TLR) expression on the mouse cornea and conjunctiva, which we hypothesize is a source of inflammatory cytokines and matrix metalloproteinases (MMP). This study examines changes in ocular surface inflammation in C57BL/6 (WT), interleukin (IL)-1R-/- and MyD88-/- (deficient in TLR and IL-1R function) mice following EDE.

Methods : EDE was induced in 6-8 week old C57BL/6 (WT), MyD88-/-, and IL-1R-/- male and female mice by subcutaneous scopolamine injection (TID) and desiccating stress for 5 days. Following treatment, tear production (phenol red thread test) and corneal fluorescein staining were assessed. Tear, conjunctiva and corneal epithelial protein samples were analyzed using mouse cytokine/chemokine multiplex magnetic bead panel assay.

Results : Following EDE treatment, WT and IL-1R-/- mice showed a significant increase in ocular surface staining, while no significant difference was found in MyD88-/- mice compared to untreated littermates. Tear production was significantly reduced in all genotypes following EDE, although both IL-1R-/- and MyD88-/- mice exhibited lower levels of baseline tear production. EDE significantly (P≤0.05) increased the levels of cytokine-induced neutrophil chemoattractant (KC) in WT corneal epithelium, which was reduced or abolished in the IL-1R-/- or MyD88-/- EDE mice respectively. After treatment, conjunctival IL-2 and IL-9 levels were decreased in WT, not changed or decreased in IL-1R-/- mice and significantly increased (P≤0.001) in MyD88-/- mice. Baseline KC, IL-2 and IL-9 were significantly (P≤0.05) reduced compared to WT and EDE in the cornea. RANTES was increased in tear samples following treatment but remained low in both IL-1R-/- and MyD88-/- mice compared to WT EDE mice.

Conclusions : The loss of functional TLRs results in reduced ocular surface damage, reduced inflammatory cytokines, and an increase in Th2 cytokines. This data suggests that TLRs play a role in modulating the inflammation and damage associated with dry eye disease.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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