Keywords: Helicobacter pylori

    Helicobacter pylori (HP) is a micro-aerobic, catalase positive uremic activity of gram-negative pylori and its survival is mainly dependent on the mucosa of the gastric antrum and gastric body, rare in the cardia mucosa. 1983 the Australian scholar Narren Mars-hall first isolated in human gastric biopsy tissue Helicobacter pylori, and that this bacterium may be chronic gastritis and peptic ulcer pathogens. Since then, people will begin a series of studies on the relationship between HP and chronic gastritis, and now a lot of evidence to support the HP chronic gastritis pathogens:

    (1) in patients with chronic gastritis HP high detection rate (50% to 80%), normal gastric mucosa rarely detected HP (0 ~ 6%), chronic active gastritis higher (up more than 90%) .
    (2) chronic gastritis, especially chronic active gastritis and serum anti-HP antibodies was significantly higher anti-HP immunoglobulin can be detected in the gastric juice.
    HP number (3) on the gastric mucosa with infiltration of polymorphonuclear leukocytes is proportional to the amount of HP infection and gastritis severity, activity and gastric epithelial damage and its extent was significantly positively related to HP adhesion more parts epithelial cell degeneration, intracellular mucin granules depleted cytoplasmic reduce a larger proportion of the nucleus and cytoplasm.
    (4) anti-HP treatment significantly improved HP cleared the inflammation of the gastric mucosa, and infection recurrence inflammation appeared.
    (5) volunteers oral suspension HP cause gastritis symptoms and pathological changes.
    (6) Preparation of HP gastritis animal models of success, HP artificial infection (Gnotobiotic suckling pig, Rhesus monkey) to be successful, HP can settle in the stomach and can lead to chronic gastritis.
    (7), autoimmune gastritis, lymphocytic gastritis and postoperative bile reflux gastritis the HP detection rate is very low, suggesting that HP is not gastritis secondary infection.

    In summary, HP may be a pathogen gastritis, at least one of the cause of chronic gastritis. HP pathogenic mechanism has not been fully elucidated, may be associated with the following factors: ① HP direct invasion of host cells in gastric mucosa and induced local tissue damage; ② HP can produce a variety of enzymes and metabolites, such as uremic enzyme and its product ammonia, peroxide disproportionation enzymes, proteolytic enzymes, phospholipase A2 and C, can damage the gastric mucosa, induced inflammatory lesions; (3) the HP promote increased gastrin secretion, resulting in high acid state, so that the gastric mucosal damage; ④ HP infection but also by immunization The reaction caused by tissue damage.