Ganesalingam Kalaivarny, Ismail Salim, Sherwin Trevor, Craig Jennifer P
Department of Ophthalmology, New Zealand National Eye Centre, The University of Auckland, Auckland, New Zealand.
Clin Exp Optom. 2019 Sep;102(5):446-454. doi: 10.1111/cxo.12849. Epub 2019 Jan 10.
Ocular surface inflammation is propagated by a complex series of molecular processes and has been implicated in the pathogenesis of dry eye disease (DED), either as a causal or a downstream effect of ocular surface disease. A state of hyperosmolarity elicits an acute immune response in DED, leading to subsequent activation of the adaptive immune response. This cascade incites dysregulation of the immune system, triggering a vicious cycle of events that causes damage to the ocular surface. Symptoms associated with these events include burning, irritation, redness, photophobia and blurred vision. The chronic nature of the disease process can cause permanent alterations to the ocular surface and adnexa. An increasing investment in treatment options, and positive outcomes with novel therapies that have received subsequent regulatory approval, lends further support to the role of inflammation in DED. This review highlights the nature and function of a range of fundamental inflammatory molecules in DED to provide the clinician with an appreciation for the ways in which these factors might be manipulated in DED management.
眼表炎症是由一系列复杂的分子过程介导的，并且在干眼病（DED）的发病机制中发挥作用，无论是作为眼表疾病的病因还是下游效应。高渗状态在DED中引发急性免疫反应，导致随后适应性免疫反应的激活。这种级联反应引发免疫系统失调，触发一系列恶性循环事件，对眼表造成损害。与这些事件相关的症状包括烧灼感、刺激感、眼红、畏光和视力模糊。疾病过程的慢性性质可导致眼表和附属器的永久性改变。对治疗方案的投入不断增加，以及新疗法获得后续监管批准后的积极成果，进一步支持了炎症在DED中的作用。本综述重点介绍了DED中一系列基本炎症分子的性质和功能，以使临床医生了解在DED管理中操纵这些因素的方式。
