Location: Children's Nutrition Research CenterTitle: ICAM-1 mediates surface contact between neutrophils and keratocytes following corneal epithelial abrasion in the mouse Author
|Gagen, Debjani - Children'S Nutrition Research Center (CNRC)|
|Laubinger, Sara - Children'S Nutrition Research Center (CNRC)|
|Li, Zhijie - Children'S Nutrition Research Center (CNRC)|
|Petrescu, Matei - Tulane School Of Medicine|
|Brown, Evelyn - University Of Houston|
|Smtih, Wayne - Children'S Nutrition Research Center (CNRC)|
|Burns, Alan - Children'S Nutrition Research Center (CNRC)|
Submitted to: Experimental Eye Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/9/2010
Publication Date: 8/14/2010
Citation: Gagen, D., Laubinger, S., Li, Z., Petrescu, M., Brown, E.S., Smith, W.C., Burns, A.R. 2010. ICAM-1 mediates surface contact between neutrophils and keratocytes following corneal epithelial abrasion in the mouse. Experimental Eye Research. 91: 676-684.
Interpretive Summary: Inflammation plays a very important role in the body’s ability to resist infections, heal injured tissue and respond to cancer. We are interested in the influence of nutrition on inflammation and we study very basic mechanisms of inflammation. In this paper we analyze how one type of white blood cell called neutrophils is able to attach to normal tissue cells as the neutrophils crawl through tissue toward a site of infection. The evidence in this paper shows that molecules called integrins are necessary for their ability to crawl. It is necessary to know the molecules involved in order to understand the effects of nutrition on inflammation.
Technical Abstract: Corneal epithelial abrasion elicits an inflammatory response involving neutrophil (PMN) recruitment from the limbal vessels into the corneal stroma. These migrating PMNs make surface contact with collagen and stromal keratocytes. Using mice deficient in PMN integrin CD18, we previously showed that PMN contact with stromal 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, a known ligand for CD18, mediates PMN contact with keratocytes during corneal wound healing. Uninjured and injured right corneas from C57Bl/6 wild type (WT) mice and ICAM-1(-/-) mice were processed for transmission electron microscopy and imaged for morphometric analysis. PMN migration, stromal thickness, and ICAM-1 staining were evaluated using light microscopy. Twelve hours after epithelial abrasion, PMN surface contact with paralimbal keratocytes in ICAM-1(-/-) corneas was reduced to approximately 50% of that observed in WT corneas; PMN surface contact with collagen was not affected. Stromal thickness (edema), keratocyte network surface area and keratocyte shape were similar in ICAM-1(-/-) and WT corneas. WT keratocyte ICAM-1 expression was detected at baseline and ICAM-1 staining intensity increased following injury. Since ICAM-1 is readily detected on mouse keratocytes and PMN-keratocyte surface contact in ICAM-1(-/-) mice is markedly reduced, the data suggest PMN adhesive interactions with keratocyte-stromal networks is in part regulated by keratocyte ICAM-1 expression.