Pathogenesis of Helicobacter pylori Infection / 대한소화기학회지
The Korean Journal of Gastroenterology
; : 159-165, 2005.
Article
em Ko
| WPRIM
| ID: wpr-70853
Biblioteca responsável:
WPRO
ABSTRACT
Helicobacter pylori (H. pylori), a long term colonizer of human stomach is known to infect a half of mankind. Gastric and duodenal ulcer, gastric adenocarcinoma and MALT lymphoma develop in a subset of infected individuals. Pathogenesis of H. pylori infection is based on the long-term host to bacterial interaction and affected by the virulence factors of the bacterium, environmental and host factors (age, sex, blood type). Mucosal inflammation is the basic principle mechanism underlying the disease development in which tissue destruction may be initiated and maintained by both the bacterial toxins (CagA, VacA, LPS) and immune responses by the host. Immune evasion with bacterial modulation of host response affects the long-term host colonization. Colonization is also affected by urease and/or motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection predisposing to carcinogenesis. Host cytokine gene polymorphism would be the one explanation for host susceptibility to peptic ulcer or gastric cancer. Investigation into the pathogenesis of H. pylori related diseases could provide an answer to the impact of chronic host to microbial interaction resulting human diseases.
Palavras-chave
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Helicobacter pylori
/
Infecções por Helicobacter
/
Gastroenteropatias
Tipo de estudo:
Etiology_studies
Limite:
Humans
Idioma:
Ko
Revista:
The Korean Journal of Gastroenterology
Ano de publicação:
2005
Tipo de documento:
Article