Pathogenesis of helicobacter pylori infection: Bacterium and host relationship

Abstract

Helicobacter pylori (H. pylori) colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, t gastric ulcer in 13%, while gastric adenocarcinoma develops in 1% of all infected individuals. Pathogenesis of H. pylori infection is related to the virulence factors of the bacterium, environmental (dietary habits, hygiene, stress) and host factors (age, sex, blood type). Colonization of the gastric mucosa is related to the motility of the bacterium, presence of lipopolysacharide (LPS) and various bacterial enzymes. Gastric mucosal injury is the result of H. pylori LPS, vacuolization cytotoxin (vacA), cytotoxin associated protein (cagA), heat shock proteins and factors responsible for neutrophil chemotaxis and activity. H. pylori colonizes the gastric mucosa and zones of ectopic gastric epithelium. H. pylori infection is transmitted via oral-oral, fecal-oral and iatrogenic way (during endoscopy). Higher prevalence of the infection is associated with lower socioeconomic level, lack of drinking water, and living in a community. Acute H. pylori gastritis is superficial pangastritis progressing into the chronic phase after 7-10 days. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection. Clearly defined factors that influence the outcome of H. pylori infection include bacterial strain, distribution of gastritis, acid secretion and gastric mucosal atrophy.Hekobacterpylori (H. pylori) kolonizuje sluznicu zeluca kod oko polovine svetske populacije. Ulkus duodenuma javlja ce kod 15-25% inficiranih osoba, ulkus zeluca kod 13%, a adenokarcinom zeluca kod 1% inficiranih osoba. Patogeneza infekcije sa N. pylori zavisi od virulencije i patogenosti bakterije, faktora sredine (higijenske i dijetetske navike, stres) i osobina domacina (starost, pol, krvna grupa). Efikasnu kolonizaciju sluznice zeluca omogucavaju pokretljivost bakterije, lipopolisaharidi {LPS) i enzimi bakterije (proteoliticki enzimi, katalaza i superoksid-dismutaza). Faktori koji izazivaju ostecenje sluznice zeluca, a nalaze ce u samoj bakteriji, jesu: LPS, vakuolizacioni citotoksin (vacA), protein udruzen sa citotoksinom (sadA), proteini toplotnog stresa i faktori hemotakse i aktivacije leukocita. N. pylori naseljava sluznicu zeluca i zone ektopicnog epitela zeluca. Infekcija ce prenosi oralno-oralnim, fekalno-oralnim i jatrogenim putem (u toku endoskopskog pregleda). Faktori rizika za sirenje infekcije su nizak socijalno-ekonomski stepen razvoja, neadekvatni higijenski uslovi zivota, zivot u zajednici, kao i konzumiranje higijenski neispravne vode za pice. Akutni gastritis izazvan N. pylori je superficijalni pangastritis koji posle sedam do deset dana prelazi u visegodisnju hronicnu fazu. Dugotrajna infekcija sa H. pylori dovodi do pojave atrofije sluznice zeluca i nastanka intestinalnemeta-plazije.Faktori koji imaju uticaja na ishod infekcijesa N.pylori, a koji su do sada definisani,jesu: bakterijski soj.distribucija gastritisa, kisela sekrecija zeluca i atrofija sluznice zeluca.