Xanthine Oxidase-Induced Inflammatory Responses in Respiratory Epithelial Cells: A Review in Immunopathology of COVID-19

Table 1

Inflammatory mechanism of uric acid.

Secretion/expression	Cell	Mechanism	Reference
IL-1	Lymphocyte	Activation of inflammasome and caspase-1 complex via P2X7 receptor	[17]
IL-1β	Macrophage	Activate the inflammasome via P2X7 signaling, and treatment with a P2X7 inhibitor reduces IL-1β release	[18]
IL-1β	Human umbilical vein endothelial cells (HUVECs)	Regulate the activation of NLRP3 inflammasome by activation of ROS and K + efflux	[19]
IL-6 and TNF-α	Human umbilical vein endothelial cells (HUVECs)	High concentrations of UA significantly increased mRNA expression and extracellular release of HMGB1 from human umbilical vein endothelial cells (HUVECs) [23]. Extracellular HMGB1 binding to RAGE activates NF-κB, which leads to proinflammation.	[21]
IL-1β	Renal tubular epithelial cells (HK-2)	UA, like Lipopolysaccharides (LPS), significantly enhanced the expression of TLR4, NLRP3, IL-1β, and ICAM-1	[22]