Ocular inflammatory responses in the EP2 and EP4 receptor knockout mice

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 E-2 , 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 E-2 , 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 E-2 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 E-2 , SDF-1, RANTES, and lipopolysaccharides.