Induction of signal transduction pathways in rat gastric epithelial cells stimulated with interleukin-1 beta

Background: Interleukin-1 beta (IL-1 beta) participates in cell growth, dif ferentiation and apoptosis via activation of several kinases in a variety o f cells. Mitogen-activated protein (MAP) kinases are important intermediate s of the signal transduction pathway from the cell surface to the nucleus, leading to activation of transcription factors. There are no reports on the effect of IL-1 beta on these pathways in gastric epithelial cells. Aim: To investigate whether IL-1 beta activates MAP kinases [extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAP kinase (p38 MAPK)] and nuclear factor (NF)-kappa B, transcription facto r, in gastric epithelial cells (RGM1). Methods: The activities of ERKs and JNKs were estimated by in-gel kinase as say, and p38 MAPK activity was measured by in vitro kinase assay at various time points (0-40 min) after addition of IL-1 beta (100 pg/mL) for 20 min. The activity of NF-kappa B was analysed using gel mobility shift assay at times from 0 to 4 h after addition of IL-1 beta. Results: Activity of ERKs was detectable at 10 min, peaked at 20 min, and c ontinued at increased levels until 40 min. Activity of both JNKs and p38 MA PK were detectable during 5-20 min, and then decreased within 40 min. Activ ation of NF-kappa B occurred at 30 min, and increased activity continued fo r 6 h. Interleukin-1 beta activated MAP kinases and NF-kappa B in RGM1 cell s. Conclusion: The activation induced by this cytokine may play an important r ole in the initiation of the inflammatory process in gastric mucosa.