TNF-α potentiates uric acid-induced interleukin-1β (IL-1β) secretion in human neutrophils
TNF-α potentiates uric acid-induced interleukin-1β (IL-1β) secretion in human neutrophils
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DOI：
10.1080/14397595.2017.1369924
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发表时间：
2018-01-01
影响因子：
2.2
通讯作者：
Migita, Kiyoshi
中科院分区：
文献类型：
--
作者：
Yokose, Kohei;Sato, Shuzo;Migita, Kiyoshi
目的：尿酸单钠（MSU）可促进人单核细胞分泌白细胞介素-1（IL-1），但NOD样受体家族pyrin domain containing 3（NLRP 3）炎性小体通路的启动信号尚不清楚。在这项研究中，我们调查的作用，肿瘤坏死因子-α（TNF-α）对MSU介导的IL-1诱导在人类neutrophils.Methods：人类中性粒细胞刺激MSU，在存在或不存在的TNF-引发。通过酶联免疫吸附测定（ELISA）方法分析细胞上清液的IL-1、IL-18和半胱天冬酶-1。采用实时PCR方法分析人中性粒细胞中Pro-IL-1 mRNA的表达。结果：TNF刺激可诱导pro-IL-1 mRNA的表达;但MSU刺激并未诱导人中性粒细胞中pro-IL-1 mRNA的表达。单独的TNF-α或MSU刺激并不导致人中性粒细胞有效的IL-1分泌，而在TNF-α致敏的中性粒细胞中，MSU刺激导致显著的IL-1和IL-18分泌。TNF-引发的中性粒细胞分泌裂解caspase-1（p20），在响应MSU stimulation.Conclusion：我们的数据表明，引发的人中性粒细胞与TNF-促进尿酸介导的IL-1分泌在没有微生物刺激。这些发现提供了深入了解痛风性关节炎中嗜酸性粒细胞介导的炎症过程。
Objective: Monosodium urate (MSU) has been shown to promote interleukin-1 (IL-1) secretion in human monocytes, but the priming signals for NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway remains elusive. In this study, we investigated the role of Tumor necrosis factor-alpha (TNF-) on MSU-mediated IL-1 induction in human neutrophils.Methods: Human neutrophils were stimulated with MSU, in the presence or absence of TNF- priming. The cellular supernatants were analyzed for IL-1, IL-18, and caspase-1 by enzyme-linked immunosorbent assay (ELISA) methods. Pro-IL-1 mRNA expressions in human neutrophils were analyzed by real-time PCR method.Results: TNF- stimulation induced pro-IL-1 mRNA expression; however, MSU stimulation did not induce pro-IL-1 mRNA expression in human neutrophils. TNF- alone or MSU stimulation did not result in efficient IL-1 secretion in human neutrophils, whereas in TNF--primed neutrophils, MSU stimulation resulted in a marked IL-1 and IL-18 secretion. TNF--primed neutrophils secreted cleaved caspase-1 (p20), in response to MSU stimulation.Conclusion: Our data demonstrate that priming of human neutrophils with TNF- promotes uric acid-mediated IL-1 secretion in the absence of microbial stimulation. These findings provide insights into the neutrophils-mediated inflammatory processes in gouty arthritis.