Tumor necrosis factor (TNF)-stimulated gene-6 (TSG-6) is upregulated in various pathophysiological contexts, where it has a diverse repertoire of immunoregulatory functions. Herein, we investigated the expression and function of TSG-6 during corneal homeostasis and after injury. Human corneas, eyeballs from BALB/c (), and mice, human immortalized corneal epithelial cells and murine corneal epithelial progenitor cells were prepared for immunostaining and real time PCR analysis of endogenous expression of TSG-6. Mice were subjected to unilateral corneal debridement or alkali burn (AB) injuries and wound healing assessed over time using fluorescein stain, confocal microscopy and histology. TSG-6 is endogenously expressed in the human and mouse cornea and established corneal epithelial cell lines and is upregulated after injury. A loss of TSG-6 has no structural and functional effect in the cornea during homeostasis. No differences were noted in the rate of corneal epithelial wound closure between BALB/c, and mice. mice presented decreased inflammatory response within the first 24 h of injury and accelerated corneal wound healing following AB when compared to control mice. TSG-6 is endogenously expressed in the cornea and upregulated after injury where it propagates the inflammatory response following chemical injury.

中文翻译：

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内源性 TSG-6 调节化学损伤后的角膜炎症

肿瘤坏死因子 (TNF) 刺激基因 6 (TSG-6) 在各种病理生理环境中上调，具有多种免疫调节功能。在此，我们研究了角膜稳态期间和损伤后 TSG-6 的表达和功能。制备人角膜、来自 BALB/c 的眼球以及小鼠、人永生化角膜上皮细胞和鼠角膜上皮祖细胞，用于 TSG-6 内源表达的免疫染色和实时 PCR 分析。对小鼠进行单侧角膜清创或碱烧伤（AB）损伤，并使用荧光素染色、共聚焦显微镜和组织学评估伤口愈合情况。 TSG-6 在人和小鼠角膜和已建立的角膜上皮细胞系中内源表达，并在损伤后上调。 TSG-6 的损失在稳态过程中不会对角膜的结构和功能产生影响。 BALB/c 和小鼠之间的角膜上皮伤口闭合率没有差异。与对照小鼠相比，AB 后小鼠在受伤后 24 小时内炎症反应减少，角膜伤口愈合加速。 TSG-6 在角膜中内源性表达，并在损伤后上调，在化学损伤后传播炎症反应。