title: Helicobacter pylori inflammation, immunity, and vaccines.
abstract: Helicobacter pylori infects almost 50% of the world population and is the major cause of gastroduodenal diseases. H. pylori colonizes the gastric mucosa, activates Toll-like and Nod-like receptors, and usually elicits a T helper 1 (Th1) type of immune response, fully polarized in peptic ulcer patients. Among several bacterial factors, the neutrophil-activating protein represents a key factor driving Th1 inflammation. A complex and fascinating balance between H. pylori and host factors takes part in the gastric niche and allows the majority of infected individuals to be without any symptom during their entire life. Novel insights into the innate and adaptive responses against H. pylori, dealing with regulatory T cells and cytokines, CTLA-4 molecule, cholesterol glucosylation, and immune evasion have been elucidated during the past year and are discussed for the development of an effective vaccine.
authors.affiliation: Department of Internal Medicine, University of Florence, Florence, Italy. delios@unifi.it
authors.forename: Mario Milco
authors.initials: MM
authors.lastname: D'Elios
authors.forename: Leif P
authors.initials: LP
authors.lastname: Andersen
mesh_terms: D000818:Animals; D001428:Bacterial Vaccines / Q000276:immunology*; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology* / Q000382:microbiology; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D016209:Interleukin-8 / Q000276:immunology; D008297:Male; D051379:Mice; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D001428:Bacterial Vaccines; D016209:Interleukin-8