May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Accumulation of Complement Components in Damaged Eyes
V. Montalvo; M.M. Campos; E.F. Wawrousek; R.A. Bush; C.E. Egwuagu; C.–C. Chan; R.N. Fariss; I. Gery
Author Affiliations & Notes
  • V. Montalvo
    NEI, NIH, Bethesda, MD
    Lab of Immunology,
  • M.M. Campos
    NEI, NIH, Bethesda, MD
    Biological Imaging Core,
  • E.F. Wawrousek
    NEI, NIH, Bethesda, MD
    Lab of Molecular and Developmental Biology,
  • R.A. Bush
    Section of Translational Research on the Retina and Macular Degeneration, NIDCD, NIH, Bethesda, MD
  • C.E. Egwuagu
    NEI, NIH, Bethesda, MD
    Lab of Immunology,
  • C.–C. Chan
    NEI, NIH, Bethesda, MD
    Lab of Immunology,
  • R.N. Fariss
    NEI, NIH, Bethesda, MD
    Biological Imaging Core,
  • I. Gery
    NEI, NIH, Bethesda, MD
    Lab of Immunology,
  • Footnotes
    Commercial Relationships  V. Montalvo, None; M.M. Campos, None; E.F. Wawrousek, None; R.A. Bush, None; C.E. Egwuagu, None; C. Chan, None; R.N. Fariss, None; I. Gery, None.
  • Footnotes
    Support  This research was supported by the Intramural Research Program of the National Eye Institute, NIH
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 5148. doi:
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      V. Montalvo, M.M. Campos, E.F. Wawrousek, R.A. Bush, C.E. Egwuagu, C.–C. Chan, R.N. Fariss, I. Gery; Accumulation of Complement Components in Damaged Eyes . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5148.

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Abstract

Purpose: : Components of complement contribute to the pathogenic process of ocular diseases, such as AMD, by being highly chemotactic and capable of facilitating neovascularization. Our study deals with accumulation of complement components in ocular tissues damaged by inflammation or light.

Methods: : Mouse eyes were damaged by the following procedures: (i) exposure of BALB/c mice to bright white light (5000 lux) for 25 hours, that caused apoptosis of retinal photoreceptors, (ii) induction of experimental autoimmune uveitis (EAU) in B10.RIII mice by immunization with IRBP; (iii) transgenic (Tg) expression, under control of the αA–crystallin promoter, of interleukin (IL)–1 or IL–7 in FVB/N mice, or interferon gamma (IFN–γ) in BALB/c. Eyes of IL–1 Tg and IL–7 Tg mice were severely inflamed, whereas eyes of IFN–γ Tg were badly damaged but had no inflammation. Healthy mice of the corresponding strains were used for controls. Accumulation of complement components was determined by immunofluorescence microscopy, using conventional procedures, with monoclonal rat antibodies against mouse C1q and C3b/iC3b/C3c.

Results: : The immunostaining patterns with antibodies against C1q and C3 were generally similar, but the intensity of staining was higher with the C3 antibody. All tested mouse eyes had complement accumulated in the choroid. Healthy eyes from all strains showed only trace or no staining in any of the other tissues. Eyes damaged by light or Tg expression of IFN–γ exhibited only low levels of complement staining in their cornea. Complement accumulated at the inflammation foci in severely inflamed eyes of IL–1 Tg, IL–7 Tg and EAU mice. In addition, the lens capsule and corneal layers of these eyes had strong staining for complement.

Conclusions: : The accumulation of complement components at inflammatory sites was expected, whereas accumulation in the cornea and lens capsule of the inflamed eyes is surprising and needs additional investigation. Lack of complement accumulation in light damaged retinas suggests that this process is not induced by apoptosis per se.

Keywords: inflammation • uveitis-clinical/animal model • immunohistochemistry 
© 2006, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2024 Association for Research in Vision and Ophthalmology.
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