Published online Sep 7, 2016. doi: 10.3748/wjg.v22.i33.7536
Peer-review started: May 8, 2016
First decision: May 20, 2016
Revised: June 29, 2016
Accepted: July 20, 2016
Article in press: July 20, 2016
Published online: September 7, 2016
To determine the impact of selected well defined Helicobacter pylori (H. pylori) antigens on gastric barrier cell turnover.
In this study, using two cellular models of gastric epithelial cells and fibroblasts, we have focused on exploring the effects of well defined H. pylori soluble components such as glycine acid extract antigenic complex (GE), subunit A of urease (UreA), cytotoxin associated gene A protein (CagA) and lipopolysaccharide (LPS) on cell turnover by comparing the wound healing capacity of the cells in terms of their proliferative and metabolic activity as well as cell cycle distribution. Toxic effects of H. pylori components have been assessed in an association with damage to cell nuclei and inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation.
We showed that H. pylori GE, CagA and UreA promoted regeneration of epithelial cells and fibroblasts, which is necessary for effective tissue healing. However, in vivo increased proliferative activity of these cells may constitute an increased risk of gastric neoplasia. In contrast, H. pylori LPS showed a dose-dependent influence on the process of wound healing. At a low concentration (1 ng/mL) H. pylori LPS accelerated of healing epithelial cells, which was linked to significantly enhanced cell proliferation and MTT reduction as well as lack of alterations in cell cycle and downregulation of epidermal growth factor (EGF) production as well as cell nuclei destruction. By comparison, H. pylori LPS at a high concentration (25 ng/mL) inhibited the process of wound repair, which was related to diminished proliferative activity of the cells, cell cycle arrest, destruction of cell nuclei and downregulation of the EGF/STAT3 signalling pathway.
In vivo H. pylori LPS driven effects might lead to the maintenance of chronic inflammatory response and pathological disorders on the level of the gastric mucosal barrier.
Core tip: This manuscript focused on the impact of Helicobacter pylori (H. pylori) antigens to the gastric mucosal barrier. We evaluated the effects of H. pylori antigens using in vitro two cellular models of gastric epithelial cells and fibroblasts, which had been independently exposed to H. pylori components. In this study, we showed different effects of subunit A of urease, cytotoxin associated gene A protein, lipopolysaccharide (LPS) as well as compounds included in a glycine acid extract on the regenerative activity of gastric epithelial cells and fibroblasts. Our results indicate deleterious, dose dependent influence of H. pylori LPS on this process.