Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host.
Helicobacter
; 28(6): e13024, 2023 Dec.
Article
en En
| MEDLINE
| ID: mdl-37798959
Helicobacter pylori (H. pylori) is a highly successful human pathogen that colonizes stomach in around 50% of the global population. The colonization of bacterium induces an inflammatory response and a substantial rise in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), mostly derived from host neutrophils and gastric epithelial cells, which play a crucial role in combating bacterial infections. However, H. pylori has developed various strategies to quench the deleterious effects of ROS, including the production of antioxidant enzymes, antioxidant proteins as well as blocking the generation of oxidants. The host's inability to eliminate H. pylori infection results in persistent ROS production. Notably, excessive ROS can disrupt the intracellular signal transduction and biological processes of the host, incurring chronic inflammation and cellular damage, such as DNA damage, lipid peroxidation, and protein oxidation. Markedly, the sustained inflammatory response and oxidative stress during H. pylori infection are major risk factor for gastric carcinogenesis. In this context, we summarize the literature on H. pylori infection-induced ROS production, the strategies used by H. pylori to counteract the host response, and subsequent host damage and gastric carcinogenesis.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Neoplasias Gástricas
/
Helicobacter pylori
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Infecciones por Helicobacter
Tipo de estudio:
Risk_factors_studies
Límite:
Humans
Idioma:
En
Revista:
Helicobacter
Asunto de la revista:
BACTERIOLOGIA
Año:
2023
Tipo del documento:
Article
País de afiliación:
China