The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis

<jats:title>Abstract</jats:title> <jats:p>Infections with the human pathogen <jats:italic>Helicobacter pylori</jats:italic> (<jats:italic>H</jats:italic>. <jats:italic>pylori</jats:italic>) can lead to severe gastric diseases ranging from chronic gastritis and ulceration to neoplastic changes in the stomach. Development and progress of <jats:italic>H</jats:italic>. <jats:italic>pylori</jats:italic>-associated disorders are determined by multifarious bacterial factors. Many of them interact directly with host cells or require specific receptors, while others enter the host cytoplasm to derail cellular functions. Several adhesins (e.g. BabA, SabA, AlpA/B, or OipA) establish close contact with the gastric epithelium as an important first step in persistent colonization. Soluble <jats:italic>H</jats:italic>. <jats:italic>pylori</jats:italic> factors (e.g. urease, VacA, or HtrA) have been suggested to alter cell survival and intercellular adhesions. Via a type IV secretion system (T4SS), <jats:italic>H</jats:italic>. <jats:italic>pylori</jats:italic> also translocates the effector cytotoxin-associated gene A (CagA) and peptidoglycan directly into the host cytoplasm, where cancer- and inflammation-associated signal transduction pathways can be deregulated. Through these manifold possibilities of interaction with host cells, <jats:italic>H</jats:italic>. <jats:italic>pylori</jats:italic> interferes with the complex signal transduction networks in its host and mediates a multi-step pathogenesis.</jats:p>