Abstract
Purpose:
Vascular endothelial growth factor (VEGF) is one of the most potent proangiogenic cytokines, which also promotes vascular permeability. However, little is known about the possible pathophysiological function of VEGF in ocular allergy. In the present study, we investigated the possible involvement of VEGF in murine ocular allergy pathogenesis.
Methods:
C57BL/6 mice were sensitized once with 100 ug ovalbumin (OVA) + pertussis toxin (300 ng) + aluminum hydroxide (1 mg). After 2 weeks, mice were challenged once/daily with OVA (250 ug) eye-drops and examined 20 min later for 10 d. Some mice received systemic VEGF receptor inhibitor (axinitib) to block VEGF function in this model. Corneal neovascularization was evaluated by FITC-CD31 antibody staining. Expressions of VEGFs at the mRNA level in the cornea and conjunctivae were evaluated by real-time PCR. Conjunctivae were also collected to enumerate eosinophil recruitment by flow cytometry.
Results:
Significant presence of corneal heme- and lymph- angiogenesis developed in this model, with increased mRNA expression of VEGF-A/C/D/R3 in the cornea and VEGF-A/D in the conjunctiva. Administration of axinitib led to reduced clinical signs of ocular allergy, as well decreased eosinophil infiltration of the conjunctiva.
Conclusions:
These results suggest that VEGF is one of the major determinants of AC and that the inhibition of VEGF may be a good therapeutic strategy.
Keywords: 609 neovascularization •
480 cornea: basic science •
475 conjunctivitis