Ocular Surface & ISPRE Ophthalmic, Genoa, Italy.
Ocular Surface and Dry Eye Center, ASST Fatebenefratelli-Sacco, Sacco Hospital - University of Milan, Milan, Italy.
Ocul Immunol Inflamm. 2021 May 19;29(4):811-816. doi: 10.1080/09273948.2021.1906908. Epub 2021 May 18.
In patients with DED, the continuous stimuli induced by excessive or persistent cold fiber sensors and overstimulation of nociceptors, as well as tear hyperosmolarity induced by evaporative stress, induce a transitory protective adaptation response called para-inflammation to restore ocular surface homeostasis. This mild subclinical inflammatory status (a type of hormetic response) can become chronic if the stimuli or tissue malfunction is present for a sustained period, causing persistent symptoms and damage to ocular surface epithelia.We review the mechanisms that characterize the transition from para-inflammation to a persistent inflammatory status of the ocular surface, including accumulation of biological waste and damaged/dysfunctional proteins, which, in normal conditions, are eliminated by autophagy, activation of the inflammasomes, and what is currently known about their role in DED pathogenesis. Furthermore, we analyze current treatments that can modulate the inflammatory response of the ocular surface and speculate about new possible therapies to treat para-inflammation.
在干燥性角结膜炎（DED）患者中，过度或持续的冷纤维传感器刺激以及由蒸发应激引起的泪液高渗，会过度刺激伤害感受器，引发一种短暂的保护性适应反应，称为类炎症反应，以恢复眼表面的稳态。如果刺激物或组织功能障碍持续存在，这种轻度亚临床炎症状态（一种类适应反应）可能会发展为慢性炎症，导致眼表面上皮持续出现症状和损伤。我们回顾了从类炎症反应到眼表面持续炎症状态的转变机制，包括生物废物和受损/功能障碍蛋白的积累，在正常情况下，这些蛋白通过自噬、炎症小体的激活而被清除，目前我们也了解到它们在 DED 发病机制中的作用。此外，我们分析了目前可以调节眼表面炎症反应的治疗方法，并推测了一些新的可能的治疗类炎症的方法。
