Helicobacter pylori in gastrointestinal disorders - Essay Example

pylori is the production of urease (Graham & Sung, 2006). H.pylori infection is typically acquired in childhood, and affects children by the age of 10-years in developing countries (Graham & Sung, 2006). In developed countries, an age-related increase in prevalence of the disease is seen (Graham & Sung, 2006). Humans are the primary reservoir of infection and the primary mode of transmission is person to person (Graham & Sung, 2006). Oral-to-oral transmission is supported by the finding of H.

pylori in dental plaque and saliva by culture and polymerase chain reaction (PCR) while fecal-to-oral transmission is supported by the finding of H. pylori in stool by culture and PCR (Graham & Sung, 2006). Gastro-oral transmission is also possible but more evidence is needed (Graham & Sung, 2006). The ability of H. pylori to colonize and damage gastric mucosal cells is determined by the immune gene polymorphisms of the host and the gastric acid secretion (Kusters, van Vliet, Kuipers, 2006).

In addition, bacterial virulence factors like the cytotoxin-associated gene pathogenicity island-encoded protein (CagA) and the vacuolating cytotoxin (VacA) help in the colonization (Kusters, van Vliet, Kuipers, 2006) and also triggers the host inflammatory response by activating the nuclear factor kappaB-dependent gene transcription (Zarrilli, Ricci, Romano, 1999). “Urease and/or motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes” are also known to affect the colonization (Lee, 2005.) The healing of the gastric mucosa is also impaired “through inhibition of epidermal growth factor receptor-dependent signal transduction pathways and induction of apoptosis” (Zarrilli, Ricci, Romano, 1999). H. pylori infection also may lead to the progression from chronic gastritis to gastric adenocarcinoma (Zarrilli, Ricci, Romano, 1999).

The “cag pathogenicity island (cagPAI), which encodes the type IV secretion