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Ocular inflammatory responses in the EP2 and EP4 receptor knockout mice
S Biswas1, P Bhattacherjee, C A Paterson
1Department of Ophthalmology & Visual Science, University of Louisville, KY, USA. s0bisw04@gwise.louisville.edu
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.
Insights
EP2 and EP4 receptors play a role in murine ocular inflammation by mediating blood-aqueous barrier disruption and leukocyte infiltration. Blocking EP2 receptors significantly inhibited these effects, while EP4 receptor blockade showed partial effects.
Area of Science:
- Ophthalmology
- Immunology
- Pharmacology
Background:
- Prostaglandin E2 (PGE2) and its receptors are implicated in inflammatory processes.
- EP2 and EP4 receptors are key mediators of PGE2 signaling.
- Understanding their role in ocular inflammation is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the specific roles of EP2 and EP4 receptors in the development of murine ocular inflammation.
- To determine the contribution of these receptors to blood-aqueous barrier disruption and leukocyte infiltration.
Main Methods:
- Utilized EP2 and EP4 receptor knockout and wild-type mice.
- Induced ocular inflammation using topical prostaglandin E2, SDF-1, RANTES, and intravitreal lipopolysaccharide.
- Assessed blood-aqueous barrier integrity by measuring aqueous humor protein levels and leukocyte counts.
- Visualized vascular leakage using fluorescein angiography.
Main Results:
- EP2 receptor knockout mice showed significant inhibition of blood-aqueous barrier disruption induced by various inflammatory stimuli.
- EP4 receptor knockout mice exhibited reduced disruption and leukocyte infiltration after lipopolysaccharide and paracentesis.
- No significant increase in aqueous humor protein was observed in EP4 knockout mice following prostaglandin E2 treatment.
Conclusions:
- EP2 and EP4 receptors partially mediate the disruption of the blood-aqueous barrier and leukocyte infiltration in ocular inflammation.
- These findings highlight the potential of targeting EP2 and EP4 receptors for managing ocular inflammatory conditions.
