Pathogenesis of Helicobacter pylori infection.
Helicobacter pylori induces chronic gastritis, the strongest known risk factor for peptic ulcer disease and distal gastric cancer, yet only a fraction of colonized individuals ever develop clinical disease. H. pylori isolates possess substantial genotypic diversity, which engenders differential host inflammatory responses that influence pathologic outcome. However, clinical sequelae are not completely dependent upon bacterial virulence factors, and disease is also influenced by host genetic diversity, particularly within immune response genes. The focus of this article will be to provide an understanding of mechanisms that underlie H. pylori persistence and pathogenesis as a framework for understanding disease processes that develop from chronic inflammation. Identification of mechanisms that regulate ongoing H. pylori-host interactions will not only improve targeted diagnostic and therapeutic modalities, but may also provide insights into other diseases that arise within the context of pathogen-initiated inflammatory states.
Peek
Richard M
RM
Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. richard.peek@vanderbilt.edu
D000942:Antigens, Bacterial / Q000276:immunology*; D001422:Bacterial Adhesion; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D005753:Gastric Mucosa / Q000382:microbiology; D005756:Gastritis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology*; D016480:Helicobacter pylori / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism*; D011110:Polymorphism, Genetic; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism
D000942:Antigens, Bacterial; D016207:Cytokines