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C.W. Smith, Z. Li; Delayed Corneal Epithelial Wound Healing in Intercellular Adhesion Molecule-1 (ICAM-1, CD54) Deficient Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2146.
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Purpose: Published reports indicate that ICAM-1-deficient mice exhibit delayed dermal wound healing. Since ICAM-1 is expressed on many different cell types at sites of injury we have begun to examine its role in corneal epithelial wound healing. Methods: Mice with a null mutation for ICAM-1 (backcrossed 10 generations to C57Bl/6J) and littermate controls were evaluated. The central corneal epithelium (3 mm in diameter) was demarcated with a trephine and removed using a blade under a stereomicroscope. To evaluate the reepithelialization by image analysis, the injured corneas were stained with fluorescein and photographed periodically until closure. In a separate set of animals, injured corneas were collected at 7 intervals up to 96 hours and assayed for interleukin-1 (IL-1) by ELISA. Results: None of the animals exhibited evidence of overt infection. A significant difference in wound healing was evident when ICAM-1 -/- and wild-type (WT) wounds were compared. WT wounds were 50% closed by 10 hours and complete within 24 hours. In contrast, ICAM-1-/- wounds were 50% closed by 17 hours and not complete until 36 hours (p<0.01). Extracts of WT corneas revealed peak IL-1 levels at 12 hours while ICAM-1-/- corneas peaked at 24 hours with levels that markedly exceeded those of WT mice. IL-1 levels returned to baseline by 48 hours in both WT and ICAM-1-/- corneas. Conclusions: These results indicate a potential role for ICAM-1 in corneal wound healing. It remains to be determined whether this relates to the signaling functions of ICAM-1 in epithelial cells, or the function of ICAM-1 as a ligand for leukocyte integrins.
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