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Induction of CD69 expression by cag PAI-positive Helicobacter pylori infection

World Journal of Gastroenterology 2011年第32期17卷 3691-3699页

作者： Naoki Mori Chie Ishikawa Masachika Senba Department of Microbiology and Oncology Graduate School of Medicine University of the Ryukyus Nishihara Okinawa 903-0215 Japan Department of Internal Medicine Omoromachi Medical Center 1-3-1 Uenoya Naha Okinawa 900-0011 Japan Transdisciplinary Research Organization for Subtropics and island Studies University of the Ryukyus Nishihara Okinawa 903-0213 Japan Department of Pathology Institute of Tropical Medicine Nagasaki University Nagasaki 852-8523 Japan

AIM: To investigate and elucidate the molecular mechanism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori ) infection. METHODS: The expression levels of CD69 in a T-cell line, Jurkat, primary human peripheral blood mononuclear cells (PBMCs), and CD4 + T cells, were assessed by immunohistochemistry, reverse transcription polymerase chain reaction, and flow cytometry. Activation of CD69 promoter was detected by reporter gene. Nuclear factor (NF)-κB activation in Jurkat cells infected with H. pylori was evaluated by electrophoretic mobility shift assay. The role of NF-κB signaling in H. pylori-induced CD69 expression was analyzed using inhibitors of NF-κB and dominant-negative mutants. The isogenic mutants with disrupted cag pathogenicity island (cag PAI) and virD4 were used to elucidate the role of cag PAI-encoding type Ⅳ secretion system and cagA in CD69 ***: CD69 staining was detected in mucosal lymphocytes and macrophages in specimens of pa- tients with H. pylori-positive gastritis. Although cag PAI- positive H. pylori and an isogenic mutant of virD4 induced CD69 expression, an isogenic mutant of cag-PAI failed to induce this in Jurkat cells. H. pylori also induced CD69 expression in PBMCs and CD4 + T cells. The activation of the CD69 promoter by H. pylori was mediated through NF-κB. Transfection of dominant-negative mutants of IκBs, IκB kinases, and NF-κB-inducing kinase inhibited H. pylori-induced CD69 activation. Inhibitors of NF-κB suppressed H. pylori-induced CD69 mRNA expression. CONCLUSION: The results suggest that H. pylori induces CD69 expression through the activation of NF-κB. cagPAI might be relevant in the induction of CD69 expression in T cells. CD69 in T cells may play a role in H. pylori-induced gastritis.

关键词： CD69 T cells Helicobacter pylori cag pathogenicity island Nuclear factor-κB

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Interleukin-1 and TNF-α polymorphisms and Helicobacter pylori in a Brazilian Amazon population

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World Journal of Gastroenterology 2009年第12期15卷 1465-1471页

作者： Hivana Patricia Melo Barbosa Luisa Caricio Martins Sidney Emanuel Batista dos Santos Samia Demachki Mnica Baraúna Assumpo Charliana Damasceno Arago Tereza Cristina de Oliveira Corvelo Laboratory of Immunogenetics Federal University of Pará66075-110BelémBrazil Nucleus of Tropical Medicine Federal University of Pará66055-240BelémBrazil Laboratory of Human and Medical Genetics Federal University of Pará66075-110BelémBrazil Department of Pathology Joo de Barros Barreto Universitary HospitalFederal University of Pará66073-000BelémBrazil Department of Endoscopy Joo de Barros Barreto Universitary HospitalFederal University of Pará66073-000BelémBrazil

AIM： To study the association between Interleukin-1 （IL-1） and tumor necrosis factor （TNF）-α polymorphisms, infection by Helicobacter pylori （H pylori） and the development of gastrointestinal diseases.METHODS： Genomic DNA was extracted from the peripheral blood of 177 patients with various gastrointestinal diseases and from 100 healthy volunteers. The polymorphisms in IL-1β and TNF-α genes were analyzed using the polymerase chain reactionrestriction fragment length polymorphism method （PCRRFLP） and those from IL-1RN with PCR. The presence of infection due to H pylori and the presence of the cagA toxin were detected by serology. The histopathological parameters in the gastric biopsies of the patients were according to the Sydney classification.RESULTS： A comparison of the frequencies of the different polymorphisms studied among the patients and the control group demonstrated that the allele IL- 1RN＊2 was more frequent among patients with gastric ulcers and adenocarcinoma. Carriers of the allele IL- RN＊2 and those with reactive serology for anti-cagA IgG had a greater risk of developing peptic ulcer and gastric adenocarcinoma, as well as a higher degree of inflammation and neutrophilic activity in the gastricCONCLUSION： Our results indicate a positive association between IL-1RN gene polymorphism and infection by positive H pylori cagA strains and the development of gastric ulcers and adenocarcinoma.

关键词： Helicobacter pylori Interleukin 1β gene Interleukin-1 receptor antagonist gene TNF-α gene cag pathogenicity island

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Helicobacter pyloristrain-specific modulation of gastric inflammation in Mongolian gerbils

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World Journal of Gastroenterology 2005年第10期11卷 1549-1553页

作者： KenOhnita HajimeIsomoto ShojiHonda AkihiroWada Chun-YangWen YoshitoNishi YoheiMizuta ToshiyaHirayama ShigeruKohno DepartmentofInternalMedicine NagasakiUniversitySchoolofMedicineSakamoto1-7-lNagasakiJapan DepartmentofInternalMedicine OitaMedicalUniversity1-1HasamaOita987-5593Japan DepartmentofBacteriology InstituteofTropicalMedicineNagasakiUniversitySchoolofMedicineSakamoto12-4NagasakiJapan DepartmentofMolecularPathology AtomicBombDiseaseInstituteNagasakiUniversitySchoolofMedicineSakamoto12-4NagasakiJapan

AIM: The cag pathogenicity island (PAI) is one of potential virulence determinants of Helicobacter pylori. The Mongolian gerbil is a suitable experimental animal for the screening of virulence factors of H ***: Five-week-old Mongolian gerbils were inoculated with a standard H pylori strain (ATCC 43504)possessing the cag PAI or a clinical isolate lacking the genes' cluster (OHPC-0002). The animals were killed at 2, 4, 8, 24 and 48 wk after inoculation (n = 5 each), and macroscopic and histopathological findings in the stomachs were ***: In gerbils infected with ATCC 43504, a more severe degree of infiltration of polynuclear and mononuclear cells and lymphoid follicles was observed from 4 wk after inoculation compared to gerbils infected with OHPC-0002 especially in the antrum and transitional zone from the fundic to pyloric gland area. In addition,glandular atrophy, intestinal metaplasia, gastric ulcer and hyperplastic polyps were noted in gerbils infected with ATCC 43504, whereas only mild gastric erosions occurred in those infected with ***: Our results indicate that the cag PAI could be directly involved in gastric immune and inflammatory responses in the Mongolian gerbils, leading to a more advanced gastric disease.

关键词： Helicobacter pylori Mongolian gerbil cag pathogenicity island

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