H. pylori inflammation: investigation of the molecular mechanisms of the inflammatory response

Published in the International Journal of Molecular Sciences a new work resulting from the collaboration of the Laboratory of Pharmacognosy with the Laboratory of Molecular Microbiology and the Laboratory of Biochemistry and Molecular Biology of Metabolism-Mass Spectrometry “Giovanni Galli” of the DiSFeB ‘Rodolfo Paoletti’. The study involved the investigation of the inflammatory response to the infection of two strains, with different virulence, of Helicobacter pylori in tumoral (AGS) and non-tumorous (GES-1) human gastric epithelial cells, comparing it with the inflammation induced by the stimulus pro-inflammatory TNF in the same cells. The aim of the work was to better characterize the GES-1 cell line in comparison with AGS, the most studied line in the inflammatory field. By analyzing the activation state of the NF-κB signaling pathway, the expression and secretion of the cytokines most involved in inflammatory phenomena and a in-depth analysis of the transcriptome, it was discovered that the inflammatory response of gastric epithelial cells to different strains of H. pylori it is triggered by the activation of multiple pathways and transcription factors, such as CCAAT/enhancer-binding proteins (CEBP), and not exclusively by the activation of NF-κB. Furthermore, by comparing the transcriptomic profiles, it was discovered that H. pylori infection induces a less potent inflammatory response in GES-1 cells compared to TNF, but influences gene transcription to a greater extent by specifically inducing transcription factors such as CEBPβ and numerous zinc-fingers protein regions.

The article is available at the following link:https://www.mdpi.com/1422-0067/24/20/15147