Helicobacter pyloriand Nucleolar Organizer Regions in the Gastric Antral Mucosa

Abstract

The association of Helicobacter pylori with an increased risk of gastric adenocarcinoma has been documented, but its mechanisms have not been elucidated. This study explored these mechanisms by addressing the relationship between H pylori and the silver-staining nucleolar organizer regions (AgNORs) in the gastric antrum. The number of AgNORs per nucleus has been correlated with proliferative rate and ploidy. The results of gastric biopsies performed before and after treatment for H pylori showed that only patients who cleared the H pylori infection had a significant decrease in the number of AgNORs per nucleus. A positive association between AgNOR counts and the severity of polymorphonuclear infiltrate could be demonstrated in patients who did not clear H pylori infection. The authors concluded that H pylori infection alters the replication cycle of the antral mucosa, inducing hyperproliferation and possibly ploidy abnormalities. Whether these alterations are induced directly by the bacterium or by the acute inflammatory infiltrate remains undecided; the data in this study suggest a possible direct effect of the polymorphonuclear leukocytes.

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

“…Increased cell proliferation has been identified as an underlying mechanism for increased mutagenesis, and possibly initiates carcinogenesis (Ames and Gold, 1990;Eidt et al, 1995); it has also been thought to be a consequence of chronic H. pylori infection (Cahill et al, 1994;Correa et al, 1994). As measuring mucosal proliferation is complicated and time-consuming, replacement of the surface epithelium by regenerative epithelium (RE) can be assessed instead, because this parameter is closely correlated with the grade of epithelial proliferation (Stolte et al, 1995).…”

Immunohistochemical assessment of Fhit protein expression in advanced gastric carcinomas in correlation with Helicobacter pylori infection and survival time.

“…H. pylori exerts its carcinogenic effect in the stomach via one of two possible mechanisms: 1. direct transformation of gastric mucosa via metabolic products, 2. rapid transformation of epithelial cells triggered by infection-induced mucosal damage, which may increase the risk of DNA destruction, thus predisposing the mucosa to transformation through absorption or endogenous mutagens and inflammatory bioproducts, e.g. peroxide and hydroxy ions [4]. The analysis of a tumour suppressor gene, i.a.…”

Increased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor κ B expression and enhanced antiapoptosis-related proteins inHelicobacter pylori-infected non-cardiac gastric adenocarcinoma

“…One possible factor is that increased inflammation generates reactive oxygen and nitrogen intermediates that have been shown to damage DNA directly [4] . Mucosal hyperproliferation has been reproducibly demonstrated in H pylori-infected human [5][6][7] and rodent gastric tissue [8][9][10] , and proliferation scores normalize following successful eradication in humans [5][6][7] . However, maintenance of tissue integrity requires that enhanced cell production is accompanied with increased rates of cell loss consequently, studies have also examined the effect of H pylori on apoptosis.…”