Allergic conjunctivitis is a common ocular surface allergic inflammatory disease triggered by hypersensitivity reactions when ocular tissues are exposed to environmental drugs or other allergens. It is divided into an early-phase reaction and a late-phase reaction. Ragweed pollen is a prevalent allergen. Upon the first exposure to the organism, allergen-specific IgE binds to FcεRI on the membrane of mast cells, inducing a sensitized state in the body. When the same allergen recontacts the sensitized organism, it cross-links with IgE anchored on FcεRI of conjunctival mast cells. Receptor crosslinking triggers mast cell degranulation and the subsequent release of multiple inflammatory mediators, thereby initiating the early-phase reaction of allergic conjunctivitis. This phase is characterized by vasodilation, increased vascular permeability and ocular pruritus, lasting for 20 to 30 minutes. Chemokines released by mast cells upregulate the expression of adhesion molecules on locally activated vascular endothelial cells and further initiate the late-phase reaction, which generally occurs 6–8 hours after allergen exposure. Histologically, the late-phase reaction is dominated by inflammatory cell infiltration, especially eosinophils. Antigen-specific T cells mediate the recruitment and migration of eosinophils to the conjunctiva, ultimately resulting in ocular tissue damage.

BALB/c mice (half male and half female, 6 weeks old)
Modeling method: Subcutaneous injection of ragweed pollen into the footpads followed by ocular challenge was performed to establish the allergic conjunctivitis model.
Positive drug: Dexamethasone
Evaluation indexes: ocular appearance score, mast cell counting, IgE level detection, HE staining

Ocular appearance score, mast cell count and IgE level