Résumé
A large body of work has been devoted to tumor necrosis factor α or interleukin‐1β (IL‐1β) signaling leading to the activation of the transcription factor nuclear factor‐κ B (NF‐κ B) in various cell types. Several studies have indicated that NF‐κ B activation depends strictly on the production of reactive oxygen intermediates. In this report, we first demonstrated that IL‐1β is a potent activator of NF‐κ B in various epithelial transformed ccll lines (OVCAR‐3, SKOV‐3, MCF7 A/Z). In these cells, IL‐1β rapidly induces NF‐κ B through a complete degradation of Iκ B‐α while H2O2 activates NF‐κ B with slower kinetics through a partial degradation of IkB‐α, p100 and p105. We showed that IL‐1β‐mediated induction of NF‐κ B in OVCAR‐3 and in other epithelial cell lines does not proceed through the production of reactive oxygen intermediates, while the same cytokine activates NF‐kB in lymphoid cells through the intracellular generation of H2O2. Our study demonstrated that several signaling pathways lead to the activation of NF‐κ B, following IL‐1β treatment in different cell types.