Neuropathic pain and itching: allergic conjunctivitis

Up to a third of the general population suffers from allergic conjunctivitis, which is quite common. The type 2 inflammatory pathway focuses on current knowledge in pathophysiology and therapeutic approaches. Since a significant majority of people with allergic conjunctivitis also experience eye itching and discomfort, there was growing evidence that neurogenic pathways can potentially contribute to allergic inflammation.

On the ocular surface, unmyelinated C-fibers can be directly triggered by mast cell mediators and mediate histaminergic irritation. In addition, TRPV1+ (histamine-dependent) and TRPA1+ (histamine-independent) neurons that exacerbate eye discomfort and itching in allergic conjunctivitis are present in the conjunctival mucosa. Moreover, the FcεRI expressed on the peripheral neurons is directly bound by the IgE complexed with the allergen. Aeroallergens present in the environment can potentially cause the release of inflammatory agents by directly stimulating neuronal nociceptors. Thus, allergic inflammation causes nerve endings to produce inflammatory and vasoactive neuropeptides, which cause cyclic 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 itching and eye discomfort due to allergic inflammation can 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.


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