Abstract
Purpose:
Allergy has an increasing prevalence and severity especially in industrialized countries. The spectrum of allergic symptoms ranges from allergic rhinitis to dermatitis to allergic conjunctivitis. Allergic conjunctivitis is an immunoglobulin E (IgE)-mediated type I allergic reaction. Because IgE is the central molecule responsible for allergic reactions, neutralizing IgE or inhibiting the IgE synthesis represents a rational approach for the treatment. We present a transgenic mouse model for allergic conjunctivitis using mice expressing a humanized high-affinity IgE receptor (B.6Cg-Fce1a(tm1Knt)Tg(FcERIa)1Bhk/J).
Methods:
Tg(FcεRIα) transgenic mice and controls were injected with subconjunctival NIP specific human-IgE (JW8, 100 nM in PBS) with subsequent intravenous allergen challenge with NIP (NIP25-BSA, 1.5 mg/ml in Saline). Allergic reaction was quantified in vivo using spectral domain anterior segment OCT (Heidelberg Engineering) and ex vivo using immunohistochemistry for monoclonal rabbit anti-mouse mast cell tryptase, polyclonal rabbit anti-human IgE and FcεRIα and HE staining.
Results:
The transgenic FcεRIα group showed a statistically significant (p<0.05) swelling of the conjunctiva using anterior segment OCT compared to the control group. The IgE binding was confirmed by immunohistochemistry which was co-localized to tryptase positive and FcεRIα positive mast cells.
Conclusions:
We present the preliminary results of a novel mouse model for allergic conjunctivitis using a transgenic mouse with a humanized FcεRIα receptor and quantify the allergic reactions using anterior segment OCT in vivo. This model will be helpful to dissect immunological pathways in allergic conjunctivitis and may be useful to develop novel therapeutic options for this common disease.