December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Participation of Innate Immune Macrophages in the Pathogenesis of Pigmentary Glaucoma in Mice
Author Affiliations & Notes
  • J Mo
    Schepens Eye Research Institute Department of Ophthalmology Harvard Medical School Boston MA
  • RS Smith
    Howard Hughes Medical Institute The Jackson Laboratory Bar Harbor ME
  • MG Anderson
    Howard Hughes Medical Institute The Jackson Laboratory Bar Harbor ME
  • SW M John
    Howard Hughes Medical Institute The Jackson Laboratory Bar Harbor ME
  • JW Streilein
    Schepens Eye Research Institute Department of Ophthalmology Harvard Medical School Boston MA
  • Footnotes
    Commercial Relationships   J. Mo, None; R.S. Smith, None; M.G. Anderson, None; S.W.M. John, None; J.W. Streilein, None. Grant Identification: NIH Grant EY05678
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3393. doi:
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    • Get Citation

      J Mo, RS Smith, MG Anderson, SW M John, JW Streilein; Participation of Innate Immune Macrophages in the Pathogenesis of Pigmentary Glaucoma in Mice . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3393.

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Abstract

Abstract: : Purpose: DBA/2J mice develop a genetically determined form of pigmentary glaucoma. The disease begins with peripheral transillumination as early as 4 months, evolves to include obvious pigment dispersion and elevated intraocular pressure by 6-8 months, and culminates in optic nerve atrophy beyond 10 months. We wished to determine whether innate immune cells (macrophages) appeared in aqueous humor of affected eyes and whether their appearance correlated with disease progression. Methods: Eyes of DBA/2J mice aged 2, 4, 7, and 10 months were evaluated clinically for evidence of inflammatory changes in anterior chamber and on surface of iris and lens, then removed, fixed, stained and examined by microscopy. Aqueous humor (AqH) was removed from eyes of similarly aged mice for analysis of content of protein and leukocytes. Results: AqH removed from eyes at 2 and 4 months of age was indistinguishable from normal AqH of other strains of normal mice such as BALB/c. By 6-7 months, when anterior chamber flare was detected clinically in many mice, AqH contained numerous leukocytes (∼250/µl), high levels of protein (∼7.5 mg/ml) and some samples tended to clot upon removal. At this time, pigment-containing macrophages were observed in the AqH and on the surface of lens and iris. By 10 months, few leukocytes were present in AqH, although protein levels in the fluid were higher (∼11 mg/ml). Conclusion: Onset of elevated pressure in this form of glaucoma is preceded by pigment dispersion, accumulation of pigment containing macrophages in the anterior segment, and breakdown of the blood:ocular barrier. Innate immune cells may participate in the pathogenesis of pigmentary glaucoma.

Keywords: 437 inflammation • 612 uveitis-clinical/animal model • 301 ACAID 
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