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-α (TNF-α). However, the precise mechanism that regulates TNF-α synthesis is still not clear. The nuclear transcription factor-κB (NF-κB) 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-κB-dependent gene expression in SCs. We also observed IκB-α/IκB-β degradation and the nuclear translocation of P65 due to LPS treatments. LPS-elicited TNF-α production in SCs was also drastically suppressed by SN50 (NF-κB inhibitor).