Neuroinflammation: The missing link between pain and immunity

Abstract

The density of corneal nerves in the cornea is the highest of the entire body. Most ocular surface diseases/injuries affect corneal neurons and are followed by a process named neurogenic inflammation, which eventually leads to pain, activation and recruitment of leukocytes and neoangiogenesis. On the other hand, leukocytes affect nerve physiology by secreting pro‐inflammatory cytokines and neuropeptides. The clinical outcome of the neuroinflammatory process is two‐faced. While immune activation is beneficial to prevent/control infections and ensure prompt wound healing, a prolonged and/or excessive neuroinflammatory response can have catastrophic consequences on corneal integrity and vision, or induce chronic pain. Clearly, a better understanding of these complex processes can have a deep impact on the treatment of highly prevalent ocular disorders, such as dry eye or infectious keratitis.