CD147 Aggravated Inflammatory Bowel Disease by Triggering NF-κB-Mediated Pyroptosis

• Published in: BioMed research international 2020, Vol.2020 (2020), p.1-8
• Main Authors: Gong, Sitang, Xu, Wanfu, Chen, Jiayu, Su, Mingmin, Xu, Yuxin, Huang, Ling, Liu, Ruitao, Xu, Zhaohui, Geng, Lanlan
• Format: Article
• Language: English
• Subjects: Apoptosis; Basigin - blood; Basigin - metabolism; Caspase-1; CD147 antigen; Cell death; Cell Line, Tumor; Cytokines; Epithelial cells; Gene Expression Regulation; Humans; IL-1β; Inflammasomes; Inflammation; Inflammatory bowel disease; Inflammatory bowel diseases; Inflammatory Bowel Diseases - blood; Inflammatory Bowel Diseases - metabolism; Inflammatory Bowel Diseases - pathology; Inflammatory diseases; Interleukin 18; Interleukin-18 - metabolism; Interleukin-1beta - metabolism; Intestine; Ischemia; Mucosa; NF-kappa B - metabolism; NF-κB protein; Phosphorylation; Proteins; Pyroptosis; Pyroptosis - genetics; Signal Transduction - genetics
• ISSN: 2314-6133; 2314-6141; 2314-6141
• DOI: 10.1155/2020/5341247

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.