The role of selenoprotein W in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte.

Abstract

Selenoprotein W (SelW) is mainly understood in terms of its antioxidant effects in the cellular defense system. Inflammation is an important indicator of animal tissue injury, and the inflammatory cells may trigger a sophisticated and well-orchestrated inflammatory cascade, resulting in exaggerated oxidative stress. To investigate the role of SelW in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte, in this report, the effects of selenium (Se) on mRNA expressions of SelW and inflammatory factors (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in the chicken immune organs (spleen, thymus and bursa of Fabricius) and cultured splenic lymphocyte treated with sodium selenite and H2O2, or knocked down SelW with small interfering RNAs (siRNAs) were examined. The results showed that Se-deficient diets effectively decreased the mRNA expression of SelW (P < 0.05), and induced a significantly up-regulation of COX-2, iNOS, NF-κB, PTGEs and TNF-α mRNA levels (P < 0.05). The histopathological analysis showed that immune tissues were obviously injured in the low-Se groups. In vitro, H2O2 induced a significantly up-regulation of the mRNA levels of inflammation-related genes (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in cultured splenic lymphocyte (P < 0.05). When lymphocytes were pretreated with Se before treated with H2O2, the inflammation-related genes were significantly decreased (P < 0.05). Silencing of SelW significantly up-regulated the inflammation-related genes (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in cultured splenic lymphocyte (P < 0.05). The results suggested that the expression levels of inflammatory factors (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) and SelW can be influenced by Se in birds. SelW commonly played an important role in the protection of immune organs of birds from inflammatory injury by the regulations of inflammation-related genes.