Down regulation of genes related to selenium signaling pathway in in-vivo transmigrated neutrophils from patients with Chronic Kidney Disease (IRM11P.627)

• Published in: The Journal of immunology (1950) Vol. 194; no. 1_Supplement; pp. 132 - 132.6
• Main Authors: Mansouri, Ladan, Moshfegh, Ali, Hylander, Britta, Jacobson, Stefan, Lundahl, Joachim
• Format: Journal Article
• Language: English
• Published: 01.05.2015
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.194.Supp.132.6

The most common causes of morbidity in patients with Chronic Kidney Disease (CKD), emerge from the dysregulation of immune system. Granulocytes are less functional, in terms of transmigration to the inflammatory sites. We analyzed the gene expression of neutrophils from peripheral blood, and in-vivo transmigrated neutrophils, collected by skin chamber technique, in CKD patients as well as healthy controls. We found that, transmigration induced a significant change in the gene expression, and kidney failure had different impacts on the gene expression of neutrophils in peripheral blood, and upon in vivo transmigration, comparing to healthy subjects. After Cluster analysis of the significant genes, and subjecting them to signaling pathways, we found selenium signaling pathway as one of those, which were significantly impaired in transmigrated neutrophils from CKD patients. This comprised down regulation of genes such as; Glutathione peroxidase-1 (GPx-1), Superoxide dismutase-2 (SOD2), Peroxiredoxin-1(PRDX1), and Selenoprotein W (SelW) gene. Selenoproteins play a major role in antioxidant defense, thus our results may indicate that the CKD patients have a deficiency in these components, leading to the oxidative stress in neutrophils, and their impairment. These findings, however, warrant further investigation, and we are currently in the process to setup an in-vitro system to analyze the effect of selenium compounds on different functions of neutrophils from CKD patients.