May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Role of Complement in Corneal Inflammation
Author Affiliations & Notes
  • J.-H. Sohn
    Ophthalmology-Retina Division, Wilmer Eye Institute, Johns Hopkins, Ellicott City, Maryland
  • P. Jha
    Ophthalmology, Jones Eye Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas
  • P. S. Bora
    Ophthalmology, Jones Eye Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas
  • N. S. Bora
    Ophthalmology, Jones Eye Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas
  • Footnotes
    Commercial Relationships  J. Sohn, None; P. Jha, None; P.S. Bora, None; N.S. Bora, None.
  • Footnotes
    Support  EY014623, EY016205, Research to Prevent Blindness, Inc. NY and the Pat & Willard Walker Eye Research Center, Jones Eye Institute, University of Arkansas for Medical Sciences (Little Rock, AR)
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 2386. doi:https://doi.org/
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    • Get Citation

      J.-H. Sohn, P. Jha, P. S. Bora, N. S. Bora; Role of Complement in Corneal Inflammation. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2386. doi: https://doi.org/.

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

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  • Supplements
Abstract

Purpose: : We have previously observed that a functionally active complement system is present in the normal cornea. This study was performed to investigate the role complement in corneal inflammation.

Methods: : Lipopolysaccharide (LPS) from Pseudomonas aeruginosa was applied to the scarified cornea of Lewis rats to induce keratitis and the animals were monitored daily for the clinical disease. Eyes were harvested at different time points for histologic analysis to determine the severity of the disease as well as the levels of complement activation products (C3 split products and MAC), cytokines, chemokines and chemokine receptors. The presence of C3 split products and MAC was detected by Western blotting and immunofluorescent staining respectively. Expression of TNF-α, IP-10, CCR 5, CXCR3, and CXCR4 during LPS induced keratitis was investigated by RT-PCR and Western blot analysis. Another set of animals with LPS-induced keratitis were treated with recombinant soluble Crry-Ig (topically), six hours post LPS treatment to explore the effect of complement inhibition on LPS induced keratitis. Control animals received a similar treatment with sterile PBS.

Results: : LPS treatment induced severe keratitis in Lewis rats. Inflammation developed within six hours post LPS treatment and peaked at 24 hours. The inflammation started to resolve after 36 hours and completely resolved by 72 hours. The animals with LPS-induced keratitis expressed high levels of C3 split products and membrane attack complex (MAC) in the eye. The mRNA and protein levels of inflammatory cytokines, chemokines and chemokine receptors such as TNF-α, IP-10, CCR 5, CXCR3, and CXCR4 were also up-regulated within the eyes of animals with LPS -induced keratitis. Treatment of Lewis rats with recombinant soluble (rs) Crry-Ig resulted in the inhibition of LPS-induced keratitis. The levels of C3 split products, MAC, TNF-α, IP-10, CCR 5, CXCR3, and CXCR4 were down-regulated in these animals.

Conclusions: : Complement activation contributes to inflammation in LPS induced keratitis and complement inhibition using soluble complement regulatory protein (rsCrry-Ig) suppresses keratitis in Lewis rats.

Keywords: cornea: basic science • inflammation • keratitis 
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