Pathogenesis of Helicobacter pylori Infection

Abstract

Helicobacter pylori induces chronic inflammation of the gastric mucosa, but only a proportion of infected individuals develop peptic ulcer disease or gastric carcinoma. Reasons underlying these observations include differences in bacterial pathogenicity as well as in host susceptibility. Numerous studies published in the last year provided new insight into H. pylori virulence factors, their interaction with the host and consequences in pathogenesis. These include the role of bacterial genetic diversity in host colonization and persistence, outer membrane proteins and modulation of adhesin expression, new aspects of VacA functions, and CagA and its phosphorylation‐dependent and ‐independent cellular effects. This article will also review the recent novel findings on the interactions of H. pylori with diverse host epithelial signaling pathways and events involved in the initiation of carcinogenesis, including genetic instability and dysregulation of DNA repair.

Local recall responses in the stomach involving reduced regulation and expanded help mediate vaccine‐induced protection against Helicobacter pylori in mice

“…This local proliferation also explains the observations of lymphoid follicles observed in the stomach after long-term infection [47]. Recently, local recall memory responses in peripheral non-lymphoid tissues at least for CD8 1 T cells have been shown to act to control herpes simplex infection [48]. Our data would indicate a similar local recall response for CD4 1 T cells occurs in the stomach for H. pylori infection.…”

“…Infection is chronic and causes a range of diseases ranging from acute to chronic gastritis, ulcers and, in a small proportion of patients, gastric adenocarcinoma [1].…”

Prevalencia de la infección por Helicobacter pylori en niños: estimando la edad de adquisición

“…Se sabe que la presencia de H. pylori en un individuo tiene relación con el nivel socioeconómico de éste, y a nivel poblacional, se asocia además con el nivel de desarrollo del país de residencia. Así, países como Gambia que se ubican en nivel de desarrollo bajo 7 , tienen una prevalencia de infección por H. pylori en niños que llega a 84% 8 , mientras que países con desarrollo muy alto como Japón, presentan una prevalencia inferior a 10% 9 . Chile se ubica entre los países con desarrollo alto según la clasificación de la ONU 7 , junto a otros como Brasil y Turquía, que presentan una prevalencia reportada en niños de 47,5% 10 y 23,9% 4 , respectivamente.…”

“…Adicionalmente, encontramos una tendencia hacia una menor prevalencia en los niveles socioeconómicos más altos, lo que concuerda con lo encontrado en estudios previos [7][8][9] , aunque en nuestro estudio no alcanzó significancia estadística. Los análisis de los distintos posibles escenarios, considerando los pacientes que no reportaron NSE, no cambiaron significativamente estas conclusiones, lo que podría explicarse por el bajo poder de la muestra para esta comparación.…”

Genes de patogenicidade de Helicobacter pylori, polimorfismos de citocinas e fatores ambientais afetam o desenvolvimento de doenças gástricas: uma visão geral

“…27 H. pylori infection promotes gastric carcinogenesis by at least five different mechanisms: (1) increased endogenous DNA damage and decrease repair activities, (2) induction of mutations in the mitochondrial DNA, (3) generation of a phenotype that induces mutations in the nuclear genome (4) disruption of the balance between cell proliferation and apoptosis and (5) induction of an intense gastric inflammatory response that lasts over decades that produces chronic oxidative stress and adaptive changes in gastric epithelial and immune cell pathobiology. 28 The gastric cancer classification by system Laurenclassifies gastric adenocarcinoma in intestinal or diffuse. 29 The intestinal-type is more frequently observed in older patients and it is linked closely to environmental and dietary risk factors.…”