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Title: Neutrophil (PMN) surface contact with keratocytes following corneal epithelial abrasion in the mouse: a novel role for ICAM-1

item BURNS, A - Baylor College Of Medicine
item LAUBINGER, S - Baylor College Of Medicine
item BROWN, E - University Of Houston
item PETRESCU, M - Tulane School Of Medicine
item SMITH, C - Children'S Nutrition Research Center (CNRC)
item LI, Z - Baylor College Of Medicine
item GAGEN, D - University Of Houston

Submitted to: Investigative Ophthalmology and Visual Science
Publication Type: Abstract Only
Publication Acceptance Date: 4/11/2009
Publication Date: 4/11/2009
Citation: Burns, A., Laubinger, S., Brown, E., Petrescu, M., Smith, C.W., Li, Z., Gagen, D. 2009. Neutrophil (PMN) surface contact with keratocytes following corneal epithelial abrasion in the mouse: a novel role for ICAM-1 [abstract]. Investigative Ophthalmology and Visual Science. 50: 2554.

Interpretive Summary:

Technical Abstract: Corneal epithelial abrasion is associated with an inflammatory response that involves PMN recruitment from the limbal vessels into the corneal stroma. Previously, in the injured mouse cornea, we showed that migrating PMNs not only make contact with collagen, but they also make extensive surface contact with stromal keratocytes. Using mice deficient in CD18 (a leukocyte-specific ß2 integrin), we also showed that PMN contact with keratocytes is CD18-dependent, while contact with collagen is CD18-independent. In the present study, we wished to extend these observations and determine if ICAM-1, an extracellular surface adhesion molecule expressed on a wide variety of cells and a known ligand for CD18, is expressed on mouse keratocytes and if it mediates PMN contact with keratocytes during corneal wound healing. Uninjured and injured right corneas from C57Bl/6 WT mice and ICAM-1 null mice were processed for transmission electron microscopy (TEM). Morphometric analysis on TEM sections was performed in the paralimbal stroma to assess keratocyte-network surface area, network shape, and PMN surface contacts with keratocytes and collagen. Stromal thickness and ICAM-1 staining were evaluated using immunofluorescence light microscopy. Statistical analysis was performed with GraphPad Prism. Twelve hours after central epithelial abrasion, the PMN surface area in contact with ICAM-1 null keratocytes was 50% of that seen in WT corneas; PMN surface contact with collagen was not affected by the absence of ICAM-1. Stromal thickness and keratocyte network surface area and network shape (surface/volume ratio) in ICAM-1 null and WT corneas were similar. Keratocyte expression of ICAM-1 was detected at baseline and ICAM-1 staining intensity increased following epithelial injury. Since ICAM-1 is readily detected on mouse keratocytes and PMN-keratocyte surface contact in ICAM-1 null mice is markedly reduced, we suggest PMN adhesion and migration on keratocyte stromal networks is regulated by keratocyte ICAM-1 expression. The fact that PMN CD18 is necessary for PMN-keratocyte surface interactions supports the concept that adhesive interactions between PMN CD18 and keratocyte ICAM-1 likely regulate PMN trafficking during corneal wound healing.