TNF-α Expression in Schwann Cells is Induced by LPS and NF-κB-Dependent Pathways

Lipopolysaccharide (LPS) is recognized by Toll-like receptor 4 and activates mitogen-activated protein kinase, which leads to the induction of proinflammatory cytokine gene expression. In vivo, Schwann cells (SCs) at the site of injury may also produce tumor necrosis factor-alpha (TNF-alpha). However, the precise mechanism that regulates TNF-alpha synthesis is still not clear. The nuclear transcription factor-kappa B(NF-kappa B) is an important transcription factor which is involved in the regulation of host immune responses. In the present study, we found that LPS possessed a comparable specific activity for activation of NF-kappa B-dependent gene expression in SCs. We also observed I kappa B-alpha/I kappa B-beta degradation and the nuclear translocation of P65 due to LPS treatments. LPS-elicited TNF-alpha production in SCs was also drastically suppressed by SN50 (NF-kappa B inhibitor).