The treatment of propofol induced the TGF-β1 expression in human endothelial cells to suppress endocytosis activities of monocytes

Propofol anesthesia and sedation are known to downregulate the functions of many hematopoietic cells, such as macrophages and neutrophils, in vivo. However, the effects of propofol on secretion of the regulatory cytokine transforming growth factor β1 (TGF-β1) in vivo are unknown. In this study, the effects of propofol on TGF-β1 expression in human peripheral blood mononuclear cells, umbilical vein endothelial cells (HUVECs), lymphocytes (Jurkat) and monocytes (THP-1) were tested. Moreover, these sera were also tested for regulatory activity on monocyte endocytosis with or without treatment with the TGF-β1 pathway inhibitor SB431542. Propofol raised levels of both total and activated TGF-β1 in propofol-treated patient sera after surgical operations. Furthermore, propofol induced secretion of latent TGF-β1 in HUVEC cells and enhanced TGF-β1 activation in THP-1 and Jurkat cells in vitro. Additionally, sera from propofol-treated patients suppressed monocyte endocytosis ex vivo, an effect that was abrogated by the TGF-β1 pathway inhibitor SB431542.

Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideResearch highlights► Patients received i.v. propofol injections, the vein endothelial cells would be induced to secrete more inactive TGF-β into blood. ► Propofol could induce especially macrophages to convert the inactive TGF-β into biological active form from the circumstance. ► After continuous circulation, propofol elevated both the total amount and active form of TGF-β in the sera. ► The increased levels of active TGF-β could turn to inhibit the activity of macrophages and might result in systemic immune suppression.