Up to one-third of the general population suffer from allergic conjunctivitis, which is quite common. The type 2 inflammatory pathway focuses on current pathophysiology knowledge and treatment approaches. Given that a significant majority of people with allergic conjunctivitis also experience ocular itching and discomfort, there was mounting evidence that neurogenic pathways may potentially contribute to allergic inflammation.
On the ocular surface, unmyelinated C fibers can be directly triggered by mast cell mediators and convey histaminergic irritation. Additionally, TRPV1+ (histamine-dependent) and TRPA1+ (histamine-independent) neurons that exacerbate ocular discomfort & itch in allergic conjunctivitis are present in the conjunctival mucosa. Additionally, FcεRI expressed on peripheral neurons is directly bound by allergen-complexed IgE. Aeroallergens in the environment can potentially cause the release of inflammatory agents by directly stimulating neuronal nociceptors. Thus, allergic inflammation causes nerve terminals to produce inflammatory and vasoactive neuropeptides, which cause cyclical dysregulation of the nervous system and increase mast cell activity. These repeated cycles cause neuronal plasticity and peripheral and central sensitization, which lower pain/itch thresholds and increase pain/itch responsiveness.
Chronic itch and discomfort in the eyes due to allergic inflammation may be caused by neurogenic processes such as peripheral and central sensitization. Finding treatment targets for people with refractory symptoms of allergic conjunctivitis may be aided by research into these pathways.
