PURPOSE To review cytokine- and chemokine-mediated mechanisms of diffuse lamellar keratitis (DLK) after lamellar corneal surgical procedures. METHODS Review of the basic science and clinical literature. RESULTS DLK can occur early or late (months to decades) after all lamellar corneal surgeries, including laser in situ keratomileusis, small incision lenticule extraction, anterior lamellar keratoplasty, and Descemet's stripping automated endothelial keratoplasty. It is most commonly triggered by epithelial injury during or after lamellar surgery, which leads to the release of interleukin (IL)-1α, IL-1β, and tumor necrosis factor (TNF)-α from the epithelium and into the stroma. These chemokines directly attract inflammatory cells into the cornea from the limbal blood vessels and also bind to receptors on keratocytes and corneal fibroblasts where myriad chemokines are upregulated that also chemotactically attract monocytes, macrophages, granulocytes, lymphocytes, and other bone marrow-derived cells into the corneal stroma. Other factors that can trigger DLK include retained blood in the interface, endotoxins and other toxins, and excessive keratocyte necrosis caused by femtosecond lasers. Infiltrating cells show a preference to enter any lamellar interface in the cornea, regardless of the time since surgery, because of the ease of movement toward the chemotactic attractants relative to the surrounding stroma with intact collagen lamellae and stromal cells that serve as relative barriers impeding motility. The mainstay of treatment is topical corticosteroids, but severe cases may also be treated with flap lift irrigation and systemic corticosteroids. CONCLUSIONS DLK can occur early or late after any lamellar corneal surgical procedure and is most commonly triggered by epithelial-stromal-bone marrow-derived cellular interactions mediated by corneal cytokines and chemokines. [J Refract Surg. 2020;36(2):124-130.].

中文翻译：

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弥漫性层状角膜炎的病理生理学和治疗。

目的探讨层状角膜外科手术后弥漫性层状角膜炎（DLK）的细胞因子和趋化因子介导的机制。方法回顾基础科学和临床文献。结果DLK可以在所有层状角膜手术后的早期或晚期（数月至数十年）发生，包括激光原位角膜磨镶术，小切口小孔晶状体切除术，前板层角膜移植术和Descemet剥离自动内皮角膜移植术。它最常见的原因是在层状手术期间或之后由上皮损伤引起，导致白细胞介素（IL）-1α，IL-1β和肿瘤坏死因子（TNF）-α从上皮释放到基质中。这些趋化因子直接将炎症细胞从角膜缘血管吸引到角膜中，并与角化细胞和角膜成纤维细胞上的受体结合，其中无数趋化因子被上调，这些趋化因子还趋化性地吸引单核细胞，巨噬细胞，粒细胞，淋巴细胞和其他骨髓来源的细胞进入角膜基质。可能触发DLK的其他因素包括界面中残留的血液，内毒素和其他毒素，以及飞秒激光造成的过度角膜细胞坏死。浸润性细胞表现出优先进入角膜任何层状界面的能力，而与手术后的时间无关，这是因为相对于周围基质而言趋化趋化性引诱剂易于移动，而完整的胶原蛋白层和基质细胞是阻碍运动的相对屏障。治疗的主要方法是局部使用皮质类固醇激素，但严重的病例也可以通过皮瓣提拉冲洗和全身性皮质类固醇激素治疗。结论DLK可以在任何层状角膜外科手术后的早期或晚期发生，并且最常见的是由角膜细胞因子和趋化因子介导的上皮-基质-骨髓衍生的细胞相互作用触发的。[J Refract Surg。2020; 36（2）：124-130。]。