Ocular Inflammatory Responses in the EP₂ and EP₄ Receptor Knockout Mice

Abstract

Purpose: To examine the role of EP₂ and EP₄ receptors in murine ocular inflammation. Methods: Prostaglandin EP₂ and EP₄ receptor knockout and wild-type mice were treated topically with prostaglandin E₂, SDF-1, and RANTES and lipopolysaccharide by intravitreal injection. Paracentesis was performed by puncturing the cornea. The increase in the level of aqueous humor protein and the number of leukocytes were measured and the vascular leakage of protein was visualized using fluorescein angiography. Results: In the EP₂ receptor knockout mice, there was significant inhibition of the disruption of the blood-aqueous barrier caused by lipopolysaccharides, paracentesis, prostaglandin E₂, SDF-1, and RANTES. Reductions in the disruption in the blood-aqueous barrier and leukocyte infiltration after lipopolysaccharide injection and paracentesis were significant, but there was no increase in the aqueous humor protein level after prostaglandin E₂ treatment in EP₄ receptor knockout mice. Conclusions: The results of the present experiments suggest that EP₂ and EP₄ receptors partly mediate the disruption of the blood-aqueous barrier and leukocyte infiltration induced by prostaglandin E₂, SDF-1, RANTES, and lipopolysaccharides.

KEYWORDS:

• Aqueous humor protein
• blood-aqueous barrier
• EP₂ receptor
• EP₄ receptor
• ocular inflammation