Abstract
The mechanisms associated with colonization of human gastroduodenal mucosa by Helicobacter pylori remain unclear. To colonize gastric-type epithelium H. pylori must enter the gastric lumen, resist damage by all bactericidal factors operating within the acidic gastric milieu, penetrate the mucus gel despite highly viscous and hydrophobic properties of the mucus layer, and, finally, secure optimal conditions for its further multiplication. Since the H. pylori microorganism has been seen freely spread throughout the entire mucus layer thickness as well as in intimate contact with surface epithelium, the interrelationship between this spiral microorganism and the mucus seems to be of paramount importance. H. pylori has been shown to affect adversely the chemical and physical properties of the mucus layer. Therefore, the mucus layer compromised by the presence of this microorganism may become an easy target for acid and peptic damage, which ultimately leads to mucosal pathology, inflammation and/or peptic ulcer disease.
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