Helicobacter pylori vs coronary heart disease-searching for connections

In this review,we discussed the findings and concepts underlying the potential role of Helicobacter pylori(H.pylori) infections in the initiation,development or persistence of atherosclerosis and coronary heart disease(CHD).This Gram-negative bacterium was described by Marshall and Warren in 1984.The majority of infected subjects carries and transmits H.pylori with no symptoms; however,in some individuals these bacteria may cause peptic ulcers,and even gastric cancers.The widespread prevalence of H.pylori infections and the fact that frequently they remain asymptomatic may suggest that,similarly to intestinal microflora,H.pylori may deliver antigens that stimulate not only local,but also systemic inflammatory response.Recently,possible association between H.pylori infection and extragastric disorders has been suggested.Knowledge on the etiology of atherosclerosis together with current findings in the area of H.pylori infections constitute the background for the newly proposed hypothesis that those two processes may be related.Many research studies confirm the indirect association between the prevalence of H.pylori and the occurrence of CHD.According to majority of findings the involvement of H.pylori in this process is based on the chronic inflammation which might facilitate the CHDrelated pathologies.It needs to be elucidated,if the infection initiates or just accelerates the formation of atheromatous plaque.

Impact of Helicobacter pylori on the healing process of the gastric barrier

AIM To determine the impact of selected well defined Helicobacter pylori(H. pylori) antigens on gastric barrier cell turnover.METHODS 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(Ure A),cytotoxin associated gene A protein(Cag A) 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. RESULTS We showed that H. pylori GE,Cag A and Ure A 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/m L) 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/m L) 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.CONCLUSION 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.