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Colonization and Infection by Helicobacter pylori in Humans
Author(s) -
Andersen Leif Percival
Publication year - 2007
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2007.00574.x
Subject(s) - colonization , biology , helicobacter pylori , microbiology and biotechnology , helicobacter pylori infection , helicobacter infections , virology , medicine , genetics
When Helicobacter pylori arrives in the human stomach, it may penetrate the mucin layer and adhere to the gastric epithelial cells or it may pass through the stomach without colonizing the mucosa. In this paper, the colonization process and the ensuing immunological response will be briefly described. Urease production is necessary for H. pylori to establish a pH‐neutral microenvironment around the bacteria. The flagella enable the bacteria to move and the shape of H. pylori makes it possible to penetrate the mucin layer where it comes into contact with the gastric epithelial cells. H. pylori contains several adhesins that enable it to adhere to the epithelial cells. This adherence activates IL‐8 which, together with bacterial antigens, attracts polymorphs and monocytes and causes acute gastritis. Antigen‐presenting cells activate lymphocytes and other mononuclear cells that are attracted to the inflamed mucosa, causing chronic superficial gastritis and initiating a cytotoxic or an antigen‐producing Th response. The infection is established within a few weeks after the primary exposure to H. pylori . After this initial colonization, many chemical, biochemical, and immunologic reactions take place that are of importance in the progress of the infection and the development of disease.