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Background   Helicobacter pylori  colonizes the human gastric mucosa, causing chronic inflammation, peptic ulcers and gastric cancer. A cascade of harmful processes results from the interaction of these bacteria with the gastric epithelium.    Aim  To investigate these processes in terms of upregulation of oxidative stress and cell apoptosis and downregulation of the pro-regenerative activity of cells.    Methods  We employed an  in vivo  guinea pig model at 7 or 28 days postinoculation with  H .  pylori , corresponding to an acute or chronic stage of infection, respectively, and an  in vitro  model of guinea pig primary gastric epithelial cells and fibroblasts treated with bacterial components: glycine acid extract (GE), urease subunit A (UreA), cytotoxin-associated gene A protein (CagA) and lipopolysaccharide (LPS). Cells were evaluated for metabolic activity (MTT reduction), myeloperoxidase (MPO) and metalloproteinase (MMP-9) secretion, lipid peroxidation (4-hydroxynonenal (4HNE)), migration (wound healing), proliferation (Ki-67 antigen) and cell apoptosis (TUNEL assay; Bcl-xL, Bax, Bcl-2 expression; caspase 3 cleavage).    Results  Significant infiltration of the gastric mucosa by inflammatory cells  in vivo  in response to  H .  pylori  was accompanied by oxidative stress and cell apoptosis, which were more intense 7 than 28 days after inoculation. The increase in cell proliferation was more intense in chronic than acute infection.  H .  pylori  components GE, CagA, UreA, and LPS upregulated oxidative stress and apoptosis. Only  H .  pylori  LPS inhibited cell migration and proliferation, which was accompanied by the upregulation of MMP-9.    Conclusions   H .  pylori  infection induces cell apoptosis in conjunction with increased oxidative stress. Elevated apoptosis protects against deleterious inflammation and neoplasia; however, it reduces cell integrity. Upregulation of cell migration and proliferation in response to injury in the milieu of GE, CagA or UreA facilitates tissue regeneration but increases the risk of neoplasia. By comparison, downregulation of cell regeneration by  H .  pylori  LPS may promote chronic inflammation.

plos one

The effect of Helicobacter pylori infection and different H. pylori components on the proliferation and apoptosis of gastric epithelial cells and fibroblasts