2021/12/14 by Romina Mayra Lasagni Vitar, Filippo Bonelli, Paolo Rama +1
Medicine · #Corneal Surgery and Treatments #Ocular Surface and Contact Lens #Pain Mechanisms and Treatments
paper · pdf · doi:10.1093/cei/uxab032
crossref issued 2021/12/14 · crossref published 2021/12/14 · crossref published-online 2021/12/14 · openalex publication_date 2021/12/14 · crossref created 2022/01/12 · openalex created_date 2022/01/25 · crossref published-print 2022/04/04 · crossref deposited 2023/11/15 · crossref indexed 2026/07/29 · openalex updated_date 2026/07/30
Most ocular diseases are associated with pain. While pain has been generally considered a mere (deleterious) additional symptom, it is now emerging that it is a key modulator of innate/adaptive immunity. Because the cornea receives the highest nerve density of the entire body, it is an ideal site to demonstrate interactions between pain and the immune response. Indeed, most neuropeptides involved in pain generation are also potent regulators of innate and adaptive leukocyte physiology. On the other hand, most inflammatory cells can modulate the generation of ocular pain through release of specific mediators (cytokines, chemokines, growth factors, and lipid mediators). This review will discuss the reciprocal role(s) of ocular surface (and specifically: corneal) pain on the immune response of the eye. Finally, we will discuss the clinical implications of such reciprocal interactions in the context of highly prevalent corneal diseases.