Rapamycin attenuates Th2-driven experimental allergic conjunctivitis.

Area of Science:

• Ophthalmology
• Immunology
• Pharmacology

Background:

• Allergic conjunctivitis involves eosinophil infiltration and Th2 immune responses.
• The mechanistic target of rapamycin (mTOR) signaling pathway's role in allergic conjunctivitis is not fully understood.

Purpose of the Study:

• To investigate the therapeutic potential of rapamycin, an mTOR inhibitor, in a mouse model of experimental allergic conjunctivitis (EAC).

Main Methods:

• Ovalbumin (OVA)-induced experimental allergic conjunctivitis (EAC) model in mice.
• Administration of rapamycin via intraperitoneal injection and topical application.
• Assessment of clinical signs, serum IgE and IgG1/G2a levels, conjunctival eosinophil and immune cell infiltration, cytokine expression, and mTOR signaling pathway activation.

Main Results:

• Rapamycin treatment significantly reduced clinical signs, serum IgE and IgG1/G2a ratio, and eosinophil infiltration in the conjunctiva.
• Rapamycin attenuated the infiltration of dendritic cells and T cells, and decreased Th1/Th2 cytokines in lymph nodes.
• Both systemic and topical rapamycin administration demonstrated comparable therapeutic effects, reducing inflammation and Th2 responses.

Conclusions:

• Rapamycin effectively suppresses key inflammatory pathways in experimental allergic conjunctivitis.
• mTOR signaling is implicated in the pathogenesis of allergic conjunctivitis.
• Rapamycin shows promise as a topical or systemic therapeutic agent for allergic conjunctivitis.