Purpose: A variety of adhesion molecules have been implicated in the inflammatory process. Antibody studies have previously implicated β2 integrins in intraocular inflammation, but antibodies may have inadequate distribution or unanticipated effects from binding to the cell surface. Methods: We studied mice with specific gene deletions for either β2 integrin or its principal ligand, intercellular adhesion molecule-1 (ICAM-1). Gene deleted mice or congenic controls were injected intravitreally with 250 ng of endotoxin. Results: Scoring inflammation on the basis of the number of leukocytes present in a representative cross-section of the eye, the absence of β2 integrin significantly reduced the inflammatory infiltrate (168±166 cells/eye section for knockouts vs. 384±212 cells/eye section for controls, (mean ± standard deviation) p <0.05). In contrast, the absence of ICAM-1 only slightly reduced the leukocytic response (90±140 cells/eye section for knockouts vs. 149±147 cells/eye section for controls, p > 0.1). The reduction in cellular infiltration was 74% in anterior segment, 77% in ciliary body, and 44% in posterior segment for β2 integrin deficient mice. Conclusion: β2 integrin contributes to leukocyte migration in endotoxin-induced uveitis but not all cells are dependent on it. ICAM-1 deficient mice also have a reduced cellular infiltrate in endotoxin-induced uveitis, but this difference did not reach statistical significance.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|Publication status||Published - Feb 15 1996|
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