NLRP12 负调控牙龈卟啉单胞菌脂多糖处理的小鼠巨噬细胞系（RAW264.7）中诱导型一氧化氮合酶（iNOS）的表达和肿瘤坏死因子-α的产生。
NLRP12 negatively modulates inducible nitric oxide synthase (iNOS) expression and tumor necrosis factor-α production in Porphyromonas gingivalis LPS-treated mouse macrophage cell line (RAW264.7).
机构信息
Department of Oral Microbiology, Faculty of Dentistry, Mahidol University, Bangkok, 10400, Thailand.
Department of Microbiology, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
出版信息
Inflamm Res. 2019 Oct;68(10):841-844. doi: 10.1007/s00011-019-01267-3. Epub 2019 Jul 10.
OBJECTIVE
The aim of the present study is to investigate the participation of NLRP12 in Porphyromonas gingivalis LPS-activated mouse macrophages.
METHODS
NLRP12-depleted mouse macrophages were stimulated with P. gingivalis LPS (1 μg/ml.). At indicated time points, the treated cells were lysed and the supernatant from treated cells was collected. Gene and protein expression of NLRP12 and iNOS were determined by RT-PCR and immunoblotting, respectively. The level of TNF-α production in the supernatant of the activated cells was determined by ELISA.
RESULTS AND CONCLUSION
NLRP12 was upregulated in response to stimulation with P. gingivalis LPS. In addition, when NLRP12 was depleted in P. gingivalis LPS-treated macrophages, an increase in TNF-α production and iNOS expression were observed when compared to those of the control cells, indicating that NLRP12 downregulates the inflammatory cytokine and antimicrobial molecule production in the macrophages.
目的
本研究旨在探讨核苷酸结合寡聚化结构域样受体蛋白 12（NLRP12）在牙龈卟啉单胞菌脂多糖激活的小鼠巨噬细胞中的作用。
方法
用牙龈卟啉单胞菌脂多糖（1μg/ml）刺激 NLRP12 耗竭的小鼠巨噬细胞。在指定的时间点，裂解处理后的细胞，并收集处理后细胞的上清液。通过 RT-PCR 和免疫印迹分别检测 NLRP12 和诱导型一氧化氮合酶（iNOS）的基因和蛋白表达。通过 ELISA 测定激活细胞上清液中 TNF-α 的产生水平。
结果与结论
NLRP12 被牙龈卟啉单胞菌脂多糖刺激而上调。此外，当在牙龈卟啉单胞菌脂多糖处理的巨噬细胞中耗竭 NLRP12 时，与对照组细胞相比，TNF-α 产生和 iNOS 表达增加，表明 NLRP12 下调了巨噬细胞中炎症细胞因子和抗菌分子的产生。
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