June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Bevacizumab lessens inflammation in an acute animal model of endotoxin-induced uveitis.
Author Affiliations & Notes
  • Salvador Mérida Donoso
    Instituto de Ciencias Biomédicas, Universidad CEU Cardenal Herrera, Valencia, Spain
  • Francisco Bosch-Morell
    Instituto de Ciencias Biomédicas, Universidad CEU Cardenal Herrera, Valencia, Spain
    Oftalmología Médica, FISABIO, Valencia, Spain
  • Amparo Navea
    Oftalmología Médica, FISABIO, Valencia, Spain
  • Footnotes
    Commercial Relationships Salvador Mérida Donoso, None; Francisco Bosch-Morell, None; Amparo Navea, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 161. doi:
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      Salvador Mérida Donoso, Francisco Bosch-Morell, Amparo Navea; Bevacizumab lessens inflammation in an acute animal model of endotoxin-induced uveitis. . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):161.

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

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Abstract

Purpose: Bevacizumab is a monoclonal IgG antibody that binds and inhibits all vascular endothelial growth factor isoforms. The aim of this study was to assess the anti-inflammatory efficacy of Bevacizumab in an experimental uveitis model upon a subcutaneous injection of lipopolysaccharide into Lewis rats, a valuable model for ocular acute inflammatory processes.

Methods: The integrity of the blood-aqueous barrier was evaluated 24 h after endotoxin-induced uveitis (EIU) by valuing two parameters: cell count and protein concentration in aqueous humors. Enzyme-linked immunosorbent assays of the aqueous humor samples were achieved to measure the levels of the diverse chemokine and cytokine proteins. The histopathology of the ocular was also considered.

Results: The inflammation observed in the anterior chamber of the eyes when Bevacizumab was administered with endotoxin was largely prevented since the aqueous humor cell infiltration substantially lowered concomitantly with a significant reduction in the uveal and vitreous histopathological grading. Th1 lymphocytes-related cytokine, Interleukin-2 values was also significantly reduced (Endotoxin group: 791,6 ± 250,9 pg/ml; Bevacizumab treated group: 303,7 ± 59,7 pg/ml; p ≤ 0.05), while protective IL-6 (Endotoxin group: 1285,0 ± 396,5 pg/ml; Bevacizumab treated group: 5205,8 ± 1412,0 pg/ml; p ≤ 0.05) and IL-10 (Endotoxin group: 208,0 ± 84,5 pg/ml; Bevacizumab treated group: 348,1 ± 160,0 pg/ml; p ≤ 0.05) cytokines values were increased. Concurrently, some related M1 macrophages chemokines displayed relevant increases, including GRO/KC (Endotoxin group: 3180,3 ± 1134,5 pg/ml; Bevacizumab treated group: 11911,1 ± 2063,7 pg/ml; p ≤ 0.05) a chemokine that could play any kind of protective role too.

Conclusions: At 24 h post-administration, Bevacizumab treatment in EIU significantly prevented the inflammation observed in the anterior chamber of the eyes since a substantial reduction was observed in cellular infiltration, concomitant with significant reduction noted in the uveal and vitreous histopathological grading. Bevacizumab treatment also reduced Th1 lymphocytes-related cytokine Interleukin-2 by around 60-70% and increased protective IL-6 and IL-10 cytokines.

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