Helicobacter pylori infection: new pathogenetic and clinical aspects

Abstract

Helicobacter pylori (H. pylori) infects more than half of the world's human population, but only 1% to 3% of infected people consequently develop gastric adenocarcinomas. The clinical outcome of the infection is determined by host genetic predisposition, bacterial virulence factors, and environmental factors. The association between H. pylori infection and chronic active gastritis, peptic ulcer disease, gastric cell carcinoma, and B cell mucosa-associated lymphoid tissue lymphoma has been well established. With the exception of unexplained iron deficiency anemia and idiopathic thrombocytopenic purpura, H. pylori infection has no proven role in extraintestinal diseases. On the other hand, there is data showing that H. pylori infection could be beneficial for some human diseases. The unpredictability of the long-term consequences of H. pylori infection and the economic challenge in eradicating it is why identification of high-risk individuals is crucial.

Keywords: Extraintestinal disorders; Gastroduodenal diseases; Helicobacter pylori; Host factors; Virulence factor.

Figure 1

Cytotoxin-associated gene pathogenicity island. CagA: Cytotoxin-associated gene A product; EPIYA: Glutamate-proline-isoleucine-tyrosine-alanine.

Figure 2

Targets of phosphorylated cytotoxin-associated gene A. Based on the article from Current Opinion in Microbiology, Hatakeyama M, SagA of CagA in Helicobacter pylori pathogenesis, 11, 30-37, Copyright (2008), with permission from Elsevier[7]. CagA: Cytotoxin-associated gene A product; NFκB: Nuclear factor κB; FAK: Focal adhesion kinase; Csk: C-terminal Src kinase.

Figure 3

Targets of non-phosphorylated cytotoxin-associated gene a product. Based on the article from Current Opinion in Microbiology, Hatakeyama M, SagA of CagA in Helicobacter pylori pathogenesis, 11, 30-37, Copyright (2008), with permission from Elsevier[7]. CagA: Cytotoxin-associated gene A product; PLC: Phospholipase C gamma; PAR1: Kinase partitioning-defective 1b; ZO-1: Zonula occludens 1; JAM: Junctional adhesion molecule A; NFκB: Nuclear factor κB; TNF-α: Tumor necrosis factor-α; IL: Interleukin.

Figure 4

Development of “hummingbird phenotype”. CagA: Cytotoxin-associated gene A product; PLC: Phospholipase C gamma; PAR1: Kinase partitioning-defective 1b; ZO-1: Zonula occludens 1.