Background. Pyroptosis, a novel form of inflammatory programmed cell death, was recently found to be a cause of mucosal barrier defect. In our pervious study, CD147 expression was documented to increase in intestinal tissue of inflammatory bowel disease (IBD). Objective. The aim of this study was to determine the function of serum CD147 in pyroptosis. Methods. The study group consisted of 96 cases. The centration of CD147, IL-1β, and IL-18 levels in serum was assessed by ELISA. Real-time PCR and WB were performed to analyze the effect of CD147 on pyroptosis. Results. In this study, our results showed that CD147 induced cell pyroptosis in intestinal epithelial cells (IECs) by enhancement of IL-1β and IL-18 expression and secretion in IECs, which is attributed to activation of inflammasomes, including caspase-1 and GSDMD as well as GSDME, leading to aggregate inflammatory reaction. Mechanically, CD147 promoted phosphorylation of NF-κB p65 in IECs, while inhibition of NF-κB activity by the NF-κB inhibitor BAY11-7082 reversed the effect of CD147 on IL-1β and IL-18 secretion. Most importantly, serum CD147 level is slightly clinically correlated with IL-1β, but not IL-18 level. Conclusion. These findings revealed a critical role of CD147 in the patients with IBD, suggesting that blockade of CD147 may be a novel therapeutic strategy for the patients with IBD.

中文翻译：

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CD147 通过触发 NF-κB 介导的细胞焦亡而加重炎症性肠病。


背景。细胞焦亡是一种新型的炎症性程序性细胞死亡，最近被发现是粘膜屏障缺陷的一个原因。在我们之前的研究中，记录到炎症性肠病 (IBD) 肠道组织中 CD147 表达增加。客观的。本研究的目的是确定血清 CD147 在细胞焦亡中的功能。方法。研究组由96例组成。通过 ELISA 评估血清中 CD147、IL- 1β和 IL-18 水平的集中度。进行实时PCR和WB来分析CD147对细胞焦亡的影响。结果。在本研究中，我们的结果表明，CD147 通过增强 IEC 中 IL-1 β和 IL-18 的表达和分泌来诱导肠上皮细胞 (IEC) 细胞焦亡，这归因于炎症小体的激活，包括 caspase-1 和 GSDMD以及 GSDME，导致聚集炎症反应。从机械角度来看，CD147 促进 IEC 中 NF- κ B p65 的磷酸化，而 NF- κ B 抑制剂 BAY11-7082 对 NF- κ B 活性的抑制则逆转了 CD147 对 IL-1 β和 IL-18 分泌的影响。最重要的是，血清CD147水平在临床上与IL- 1β有轻微相关，但与IL-18水平无关。结论。这些发现揭示了CD147在IBD患者中的关键作用，表明阻断CD147可能是IBD患者的一种新的治疗策略。