November 1992
Volume 33, Issue 12
Free
Articles  |   November 1992
Adhesion molecules in experimental phacoanaphylactic endophthalmitis.
Author Affiliations
  • G O Till
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
  • S Lee
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
  • M S Mulligan
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
  • J R Wolter
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
  • C W Smith
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
  • P A Ward
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
  • G E Marak, Jr
    Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
Investigative Ophthalmology & Visual Science November 1992, Vol.33, 3417-3423. doi:
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    • Get Citation

      G O Till, S Lee, M S Mulligan, J R Wolter, C W Smith, P A Ward, G E Marak; Adhesion molecules in experimental phacoanaphylactic endophthalmitis.. Invest. Ophthalmol. Vis. Sci. 1992;33(12):3417-3423.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Intraocular accumulation of inflammatory neutrophils is an important feature of experimental phacoanaphylactic endophthalmitis (EPE). Increasing evidence suggests that localization of neutrophils to the site of inflammation requires the participation of neutrophil and endothelial adhesion molecules. These studies were undertaken to determine if blocking of adhesion molecules on neutrophils (CD18) or endothelium (ELAM-1) could attenuate EPE in Lewis rats. Treatment of experimental animals with anti-CD18 or anti-ELAM-1 significantly suppressed intraocular neutrophil accumulation, retinal hemorrhage, and vasculitis, and attenuated retinal edema formation by 48% and 70%, respectively. These observations demonstrate that antibodies directed against adhesion molecules on the neutrophil (CD18) or the vascular endothelial cell (ELAM-1) exhibit potent anti-inflammatory effects, resulting in a striking amelioration of injury in EPE in rats.

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