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Updated: Jul 19, 2026
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
Published on: August 4, 2022
Modulation of ocular inflammatory responses by EP1 receptors in mice
S Biswas1, P Bhattacherjee, C A Paterson
1Department of Ophthalmology and Visual Science, University of Louisville, 301E Muhammad Ali Blvd, Louisville, KY 40202, USA. s0bisw04@gwise.louisville.edu
Abstract:
The purpose of the study was to investigate the role of EP1 receptors in intraocular inflammation and to determine possible interplay between EP1, EP2 and EP4 receptors. The eyes of separate groups of EP1 receptor knockout and wild type mice were: 1) treated topically with prostaglandin E2 (PGE2) or the EP2 receptor selective agonist, butaprost; 2) given intravitreal injection of LPS; or 3) paracentesis performed. Another group of knockout mice were pretreated topically with an EP4 receptor selective antagonist prior to paracentesis or LPS treatment. Results demonstrated a significant increase (50% or more) in the protein levels of aqueous humor of the EP1 knockout mice in response to PGE2, paracentesis or LPS. The leukocyte infiltration in the aqueous humor of the knockout mice was 47% higher when compared with that in the wild type controls in response to LPS injection. No significant change was observed in the protein levels in response to butaprost. Pretreating the knockout mice with an EP4 receptor antagonist prior to paracentesis and LPS treatment substantially reduced the aqueous humor protein levels. Also, the leukocyte count in the aqueous humor of the knockout mice in response to LPS was reduced 4 fold after pretreatment with EP4 receptor antagonist when compared with the findings in knockout mice receiving LPS only. We concluded that EP1 receptor has no modulatory effect on EP2 receptors but there is definitely cross-talk between EP1 and EP4 receptors.
Insights
EP1 receptors play a key role in intraocular inflammation, interacting with EP4 receptors. EP1 receptor knockout mice showed increased inflammation markers, which were reduced by EP4 receptor antagonist treatment.
Area of Science:
- Ophthalmology
- Immunology
- Pharmacology
Background:
- Intraocular inflammation is a significant cause of vision loss.
- Prostaglandin E2 (PGE2) receptors, including EP1, EP2, and EP4, are implicated in ocular inflammatory processes.
- Understanding receptor interactions is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of EP1 receptors in experimental intraocular inflammation.
- To explore potential cross-talk between EP1, EP2, and EP4 receptors in the eye.
Main Methods:
- Utilized EP1 receptor knockout and wild-type mice models.
- Induced intraocular inflammation via topical prostaglandin E2 (PGE2), intravitreal LPS injection, or paracentesis.
- Administered EP2 and EP4 receptor selective agonists/antagonists.
- Quantified aqueous humor protein levels and leukocyte infiltration.
Main Results:
- EP1 receptor knockout mice exhibited significantly increased aqueous humor protein levels and leukocyte infiltration following inflammatory stimuli (PGE2, LPS, paracentesis).
- EP2 receptor activation did not significantly alter protein levels.
- Pretreatment with an EP4 receptor antagonist markedly reduced protein levels and leukocyte infiltration in EP1 knockout mice.
Conclusions:
- EP1 receptors are critical in modulating intraocular inflammation.
- There is significant cross-talk between EP1 and EP4 receptors in the context of ocular inflammation.
- EP1 receptors do not appear to modulate EP2 receptor function.
