Impact ofHelicobacter pylorion the healing process of the gastric barrier

Abstract

AIMTo determine the impact of selected well defined Helicobacter pylori (H. pylori) antigens on gastric barrier cell turnover.METHODSIn 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.RESULTSWe 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.CONCLUSIONIn 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.

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

“…Gastric lesions associated with H. pylori, with exposure to acid or pepsin, are amplified and more aggressive [27]. In vivo studies indicate that the presence of H. pylori may lead to the maintenance of chronic inflammatory responses, as well as to other pathological disorders in the stomach mucosa [35].…”

Autoantibodies to a specific peptide epitope of human Hsp60 (ATVLA) with homology to Helicobacter pylori HspB in H. pylori‐infected patients

“…It is possible that the immune cells of CHD patients infected with H. pylori carrying HspB similar to human Hsp60 may respond by anti‐Hsp60 antibody production and breaking tolerance against autologous Hsp60. Due to the intake of low doses of acetylsalicylic acid by CHD patients, which impairs the gastric epithelial homeostasis, the risk of H. pylori infection can be increased . Hsp60, which is upregulated in atherogenic lesions can be targeted by anti‐Hsp60 IgG or Hsp60 specific T cells in situ and in the blood stream.…”

“…The role of H. pylori in extragastric diseases including immune thrombocytopenic purpura (ITP), iron deficiency anemia (IDA), vitamin B12 deficiency, cardiovascular diseases, diabetes mellitus, dermatological and neurologic disorders as well as lung cancer was suggested . One concept links these extragastric diseases with molecular mimicry between human and H. pylori compounds released from lysed bacteria , which destroy the gastric barrier and induce humoral and cellular immune responses deleterious to the host . A well‐documented example of cross‐reactivity caused by antigenic mimicry is Guillan‐Barre Syndrome, a neurodegenerative disease linked to Campylobacter jejuni infection .…”

Effectiveness of Citrus Fruits on Helicobacter pylori

“…A strong association between cagA and vacA signal sequence type s1 has been reported with strains carrying s1 m1 mosaic combination being able to secrete a vacuolating cytotoxin [56, 62]. A recent investigation on the impact of H. pylori antigens to the gastric mucosal barrier demonstrated a deleterious dose-influence effect of the lipopolysaccharide (LPS) [63]. The current treatment for H. pylori uses a combination of antimicrobial and antiacid agents [64].…”