Different Pathophysiology of Gastritis in East and West? A Western Perspective.

Background: Gastritis results from multifactorial gastric mucosal injury. is the main cause, and associated diseases have typical underlying patterns of gastritis. Gastric ulcer and gastric cancer (GC) develop from chronic atrophic corpus gastritis (CAG) which therefore represents the most important pattern.

[Dyspepsia, Ulcer Disease – Helicobacter pylori, Gastroesophageal Reflux Disease].

Prevalence of H. pylori (HP) is declining, whereas reflux disease and the proportion of non-steroidal antiinflammatory drugs (NSAR) to HP-induced ulcers increase. Eradication heals HP-ulcer disease, interrupts cancerous progression and can improve dyspeptic symptoms.

Host Lewis phenotype-dependent Helicobacter pylori Lewis antigen expression in rhesus monkeys.

Both human and H. pylori populations are polymorphic for the expression of Lewis antigens. Using an experimental H.

Helicobacter pylori modulates the T helper cell 1/T helper cell 2 balance through phase-variable interaction between lipopolysaccharide and DC-SIGN.

The human gastric pathogen Helicobacter pylori spontaneously switches lipopolysaccharide (LPS) Lewis (Le) antigens on and off (phase-variable expression), but the biological significance of this is unclear. Here, we report that Le+ H. pylori variants are able to bind to the C-type lectin DC-SIGN and present on gastric dendritic cells (DCs), and demonstrate that this interaction blocks T helper cell (Th)1 development.