Adiponectin antagonises LPS‐regulated secretion of inflammatory factors in airway epithelial cells, and its expression is regulated by many factors. (8th November 2020)

• Record Type: Journal Article
• Authors: Liu, Hu; Tang, Huo‐yan; Wang, Rui‐ying; Xu, Jian‐ying
• Is Part Of: Cell biochemistry and function. Volume 39:Number 1(2021)
• Page Start: 139
• Page End: 147
• Publication Date: 2020-11-08
• Subjects: adiponectin -- bronchial epithelial cells -- chronic obstructive pulmonary disease -- inflammation; Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3603
• Languages: English
• ISSNs: 0263-6484

Abstract

Abstract : Many studies have shown that adiponectin is closely related to chronic obstructive pulmonary disease (COPD), but the specific role of adiponectin in COPD is still not well understood. Adiponectin and IL‐6 expression in patients with acute exacerbation of COPD (AECOPD) was detected by ELISA. Human bronchial epithelial cells (HBECs) were stimulated with TNF‐α, IL‐6, apoptotic cells or LPS. Then, the expression of adiponectin was detected by qRT‐PCR and western blotting, and pro‐ and anti‐inflammatory factors were detected by ELISA. Adiponectin expression in AECOPD patients increased after treatment. TNF‐α and apoptotic cells promoted adiponectin expression in HBECs in a dose‐dependent manner, and apoptotic cells significantly promoted adiponectin secretion. IL‐6 also promoted adiponectin expression, but it inhibited adiponectin expression at high doses and with long treatment times. LPS inhibited adiponectin expression, but when HBECs were pretreated with anti‐TNF‐α and then treated with LPS, the expression and secretion of adiponectin increased significantly with increasing anti‐TNF‐α concentrations. Adiponectin stimulated the secretion of pro‐inflammatory factors in HBECs, but this effect was not concentration dependent. Adiponectin promoted the secretion of anti‐inflammatory factors in a dose‐dependent manner. Although LPS also stimulated HBECs to secrete pro‐inflammatory and anti‐inflammatory factors, adiponectin inhibited LPS‐induced pro‐inflammatory factor secretion and enhanced anti‐inflammatory factor secretion. Many factors regulate the expression and secretion of adiponectin, and adiponectin regulates the balance of the inflammatory response and inhibits further expansion of inflammation. Significance of the study: Many studies have shown that adiponectin is closely related to chronic obstructive pulmonary disease (COPD), but the specific role of adiponectin in COPD is still not well understood. Adiponectin expression in AECOPD patients increased after treatment. TNF‐α, IL‐6 and apoptotic cells promoted adiponectin expression in HBECs. Adiponectin stimulated the secretion of pro‐inflammatory factors in HBECs, but this effect was not concentration dependent. Adiponectin promoted the secretion of anti‐inflammatory factors in a dose‐dependent manner. Adiponectin inhibited LPS‐induced pro‐inflammatory factor secretion and enhanced anti‐inflammatory factor secretion. Therefore, many factors regulate the expression and secretion of adiponectin, and adiponectin regulates the balance of the inflammatory response and inhibits further expansion of inflammation.