Department of Visual Sciences, Division of Ophthalmology, Nihon University School of Medicine, Tokyo, Japan.
Sci Rep. 2019 Jul 3;9(1):9596. doi: 10.1038/s41598-019-46116-9.
We evaluated the role of NLR family pyrin domain containing 3 (NLRP3) inflammasome in sterile corneal inflammation caused by lipopolysaccharide (LPS) or alkali burns in C57BL6 mice or NLRP3 KO (Nlrp3) mice. Various molecules related to the NLRP3 inflammasome were upregulated in C57BL6 mice after both alkali burn injury and LPS treatment. After alkali burn injury, the corneal opacity grade was significantly reduced in Nlrp3 mice compared with C57BL6 mice. In Nlrp3 mice, Gr-1 immunoreactivity and MMP-9 mRNA expression in the corneal stroma were significantly reduced by both LPS treatment and alkali burn injury. Quantitative PCR and immunohistochemistry revealed that IL-1β and MMP-9 expression in the corneal stroma were down-regulated in Nlrp3 mice with both alkali burn injury and LPS treatment. These findings suggest that the NLRP3 inflammasome has a pro-inflammatory effect in the cornea by recruiting neutrophils to sites of inflammation.
我们评估了核苷酸结合寡聚化结构域样受体蛋白 3（NLRP3）炎性小体在脂多糖（LPS）或碱烧伤引起的 C57BL6 小鼠或 NLRP3 敲除（Nlrp3）小鼠无菌性角膜炎症中的作用。在 C57BL6 小鼠的碱烧伤损伤和 LPS 处理后，与 NLRP3 炎性小体相关的各种分子均上调。与 C57BL6 小鼠相比，Nlrp3 小鼠的碱烧伤损伤后的角膜混浊程度显著降低。在 Nlrp3 小鼠中，LPS 处理和碱烧伤损伤均显著降低了角膜基质中的 Gr-1 免疫反应性和 MMP-9mRNA 表达。定量 PCR 和免疫组织化学显示，在 LPS 处理和碱烧伤损伤的 Nlrp3 小鼠中，角膜基质中的 IL-1β 和 MMP-9 表达下调。这些发现表明 NLRP3 炎性小体通过募集中性粒细胞到炎症部位在角膜中发挥促炎作用。
