April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
High Mobility Group Box Protein-1 in Experimental Autoimmune Uveoretinitis
Author Affiliations & Notes
  • Y. Sato
    Division of Radioisotope Research,
    Kyorin University, Mitaka, Japan
  • T. Watanabe
    Department of Ophthalmology,
    Kyorin University, Mitaka, Japan
  • H. Keino
    Department of Ophthalmology,
    Kyorin University, Mitaka, Japan
  • A. Kudo
    Department of Anatomy,
    Kyorin University, Mitaka, Japan
  • H. Kawakami
    Department of Anatomy,
    Kyorin University, Mitaka, Japan
  • A. A. Okada
    Department of Ophthalmology,
    Kyorin University, Mitaka, Japan
  • Footnotes
    Commercial Relationships  Y. Sato, None; T. Watanabe, None; H. Keino, None; A. Kudo, None; H. Kawakami, None; A.A. Okada, None.
  • Footnotes
    Support  Grant-in-Aid 17791258 for Scientific Research
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 827. doi:
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      Y. Sato, T. Watanabe, H. Keino, A. Kudo, H. Kawakami, A. A. Okada; High Mobility Group Box Protein-1 in Experimental Autoimmune Uveoretinitis. Invest. Ophthalmol. Vis. Sci. 2009;50(13):827.

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

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Abstract

Purpose: : To investigate whether high mobility group box protein-1 (HMGB-1), acting as a novel proinflammatory cytokine, is involved in experimental autoimmune uveoretinitis (EAU).

Methods: : HMGB-1 concentration was measured in aqueous humor and serum obtained from Lewis rats immunized with interphotoreceptor retinoid binding protein (IRBP) peptide (R14) and complete Freund’s adjuvant (CFA), rats immunized with CFA, and non-treated rats on day 14 after immunization. Immunofluorescence histochemistry was performed to examine localization of HMGB-1 and the receptor for advanced glycation end products (RAGE) in eyes obtained from non-treated rats or EAU-induced rats.

Results: : The level of HMGB-1 in aqueous humor was significantly elevated in eyes with EAU, and both HMGB-1 and TNF- levels correlated with active ocular inflammation. HMGB-1 was expressed in the iris, ciliary body and retina of eyes from non-treated rats and EAU-induced rats. Furthermore, HMGB-1 and RAGE were found in inflammatory cells infiltrating into the anterior chamber, vitreous cavity, and subretinal space in EAU-induced rats. Some HMGB-1 or RAGE positive cells in eyes with EAU were CD68 positive.

Conclusions: : HMGB-1 was found to be elevated in the aqueous humor of eyes with EAU. Inflammatory cells infiltrating ocular tissues expressed both HMGB-1 and RAGE. These results support the possibility that extracellularly-released HMGB-1 acts as a novel proinflammatory cytokine to promote and amplify ocular inflammation in autoimmune uveoretinitis.

Keywords: uveitis-clinical/animal model • inflammation • aqueous 
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