| Full text | |
| Author(s): |
Marcelo Sady Plácido Ladeira
[1]
;
Daisy Maria Fávero Salvadori
[2]
;
Maria Aparecida Marchesan Rodrigues
[3]
Total Authors: 3
|
| Affiliation: | [1] Universidade Estadual Paulista. Faculdade de Medicina de Botucatu. Departamento de Patologia
[2] Universidade Estadual Paulista. Faculdade de Medicina de Botucatu. Departamento de Patologia
[3] Universidade Estadual Paulista. Faculdade de Medicina de Botucatu. Departamento de Patologia
Total Affiliations: 3
|
| Document type: | Journal article |
| Source: | Jornal Brasileiro de Patologia e Medicina Laboratorial; v. 39, n. 4, p. 335-342, 2003-00-00. |
| Field of knowledge: | Biological Sciences - Genetics |
| Abstract | |
Helicobacter pylori (H. pylori)-infection causes persistent inflammation with different clinical outcomes in humans, including chronic gastritis, peptic ulcer, and gastric cancer. The key determinants of these outcomes are the severity and distribution of the H. pylori-induced inflammation. Recent evidence has demonstrated that H. pylori strains possess genotypic diversity whose products trigger inflammatory process and the main mediators and cytokines, which may engender differential host inflammatory responses with distintict clinical outcomes. H. pylori strains that possess the cag pathogenecity island induce more severe inflammation via activation of gene transcription, thus enhancing the risk for peptic ulcer and distal gastric cancer. The oxidative and nitrosative stress induced by inflammation plays an important role in gastric carcinogenesis as a mediator of carcinogen formation, DNA damage, and imbalances between cell proliferation and apoptosis. (AU) | |