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Recurrent Herpetic Stromal Keratitis in Mice, a Model for Studying Human HSK
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Spontaneous bacterial keratitis in CD36 knockout mice.

Julia Klocke1, Rita N Barcia, Susan Heimer

  • 1Department of Ophthalmology, Harvard Medical School, Boston, MA, USA.

Investigative Ophthalmology & Visual Science
|September 18, 2010
PubMed
Summary

CD36 is crucial for maintaining the corneal epithelial barrier. Mice lacking CD36 spontaneously develop bacterial keratitis due to barrier breakdown and increased bacterial binding.

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Area of Science:

  • Ophthalmology
  • Immunology
  • Microbiology

Background:

  • CD36, a scavenger receptor, is present in the corneal epithelium and involved in barrier homeostasis.
  • The role of CD36 in protecting the cornea from infection is not fully understood.

Purpose of the Study:

  • To investigate if CD36 is essential for maintaining the corneal epithelial barrier against infection.
  • To determine if CD36-deficient mice exhibit increased susceptibility to bacterial keratitis.

Main Methods:

  • Corneas from CD36(-/-), TSP1(-/-), TLR2(-/-), and wild-type mice were examined.
  • Epithelial tight junctions and mucin layer integrity were assessed.
  • Bacterial binding and quantification were performed using Staphylococcus aureus and Staphylococcus xylosus.

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Main Results:

  • CD36(-/-) mice developed spontaneous corneal defects with age, including disrupted tight junctions and mucin layers.
  • These defects were associated with macrophage infiltration and increased bacterial binding.
  • Elevated levels of Staphylococcus xylosus were found in CD36(-/-) corneas with severe defects.

Conclusions:

  • CD36 deficiency leads to spontaneous bacterial keratitis in mice, independent of TLR2 and TSP1.
  • CD36 is critical for corneal epithelial barrier function, preventing bacterial adhesion and subsequent infection.
  • This study reports the first instance of spontaneous bacterial keratitis in a mouse model.