title: Helicobacter pylori-induced immunological responses in patients with duodenal ulcer and in patients with cardiomyopathies.
abstract: The interaction between the bacteria and the host is a key factor determining the clinical consequences of H. pylori infection. The immune system plays an important role in either promoting or preventing the disease. The mucosal production of TNF-alpha, IL-6, IL-8 and IL-10 and the CagA status were investigated in H. pylori-positive patients with duodenal ulcer (DU). The concentrations of these cytokines in gastric antral mucosal specimens from patients infected with H. pylori (n = 40) were determined by ELISA and compared with data on mucosal specimens from H. pylori-negative patients (n = 12). The local TNF-alpha, IL-6 and IL-8 concentrations in the antral biopsy samples were significantly higher (p < 0.001) in the patients infected with H. pylori than in the samples from the H. pylori-negative subjects. CagA positivity was demonstrated in 39 (97.5%) of the 40 patients with DU, and in 41 (70.7%) of H. pylori-positive (58 of 100) healthy blood donors. In complementary studies focusing on extragastric disease, it was found that 57% of patients with ischaemic heart disease were seropositive as concerns H. pylori, and 91% of them had antibodies against human heat shock protein 60, too. This study suggests that, besides the bacterial virulence factor, the host response of an increased mucosal production of inflammatory cytokines can be relevant to the gastric pathophysiology in H. pylori-induced DU. At the same time, in ischaemic heart diseases the role of autoimmune processes induced by H. pylori cannot be excluded.
authors.affiliation: Department of Medical Microbiology and Immunobiology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
authors.forename: G
authors.initials: G
authors.lastname: Klausz
authors.forename: Andrea
authors.initials: A
authors.lastname: Tiszai
authors.forename: Zsuzsa
authors.initials: Z
authors.lastname: Lénárt
authors.forename: Zsófia
authors.initials: Z
authors.lastname: Gyulai
authors.forename: L
authors.initials: L
authors.lastname: Tiszlavicz
authors.forename: Márta
authors.initials: M
authors.lastname: Hogye
authors.forename: M
authors.initials: M
authors.lastname: Csanády
authors.forename: J
authors.initials: J
authors.lastname: Lonovics
authors.forename: Yvette
authors.initials: Y
authors.lastname: Mándi
mesh_terms: D000942:Antigens, Bacterial / Q000276:immunology*; D009202:Cardiomyopathies / Q000150:complications / Q000276:immunology* / Q000382:microbiology; D004381:Duodenal Ulcer / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D005753:Gastric Mucosa / Q000276:immunology; D016481:Helicobacter Infections / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D007378:Interleukins / Q000096:biosynthesis* / Q000097:blood / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000378:metabolism
chemical_list: D000942:Antigens, Bacterial; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha