3.3.2 Innate Immunity Activation Due to H. pylori -- 3.3.3 Adaptive Immunity Activation Due to H. pylori -- 3.3.4 Interaction of H. pylori with Tight Junction Proteins -- 3.4 Conclusion -- References -- 4: Change of Acid Secretions, Ghrelin, and Leptin, by H. pylori -- 4.1 Introduction -- 4.2 Gastric Acid Secretion and H+, K+-ATPase with Regard to H. pylori Infection -- 4.2.1 Gastric Acid Secretion and H+, K+-ATPase -- 4.2.2 Effect of H. pylori Infection on the Gastric Acid Secretion -- 4.2.2.1 Acute Phase of H. pylori Infection Causes Hypochlorhydria -- 4.2.2.2 Effect of H. pylori Infection on H+, K+-ATPase -- 4.2.2.3 Interaction Between H. pylori Infection and Gastric Acid Secretion Determining the Pattern of Gastritis -- 4.2.2.4 Chronic Phase of H. pylori Infection and Gastric Acid Secretion -- 4.2.2.5 Gastrin and Somatostatin in Regard to H. pylori Infection -- 4.2.3 Effect of H. pylori Eradication on Gastric Acid Secretion -- 4.3 Ghrelin -- 4.3.1 Role of Ghrelin -- 4.3.2 Regulation of Ghrelin in Regard to H. pylori Infection -- 4.3.3 Effect of Eradication of H. pylori on Ghrelin -- 4.4 Leptin -- 4.4.1 Regulation and Role of Gastric Leptin -- 4.4.2 Regulation of Leptin in Regard to H. pylori Infection -- 4.5 Conclusions -- References -- 5: H. pylori Virulence Factors: Toxins (CagA, VacA, DupA, OipA, IceA) -- 5.1 Introduction -- 5.2 Cytotoxin-Associated Gene A (CagA) -- 5.2.1 cag Pathogenicity Island (cag PAI) -- 5.2.2 Diversity of the cagA Gene -- 5.2.3 The Relevance Between the EPIYA Segment and Pathogenicity of CagA -- 5.2.4 Tyrosine Phosphorylation of CagA -- 5.2.5 Phosphorylation-Independent Signaling of CagA -- 5.3 Vacuolating Cytotoxin (VacA) -- 5.3.1 VacA Structure -- 5.3.2 vacA Gene Diversity -- 5.3.3 vacA Genotype in Relation to Gastroduodenal Diseases -- 5.3.4 Biological Functions of VacA. |
5.4 Outer Membrane Inflammatory Protein (OipA) -- 5.5 Induced by Contact with Epithelium (IceA) -- 5.6 Duodenal Ulcer Promoting Gene (dupA) -- 5.7 Other Virulence Factors -- 5.7.1 Shape Switch -- 5.7.2 High-Temperature Requirement A (HtrA) and Heat-Shock Proteins (Hsps) -- 5.7.3 Arginase -- 5.7.4 Catalase and Superoxidase Dismutase (SOD) -- 5.7.5 Cholesteryl α-Glucosyltransferase -- 5.8 Conclusion -- References -- 6: H. pylori Virulence Factors: Genetic Polymorphism and Disease -- 6.1 Introduction -- 6.2 Cytotoxin-Associated Gene A (cagA) -- 6.2.1 cagA Type: Western Versus East Asian -- 6.3 Vacuolating Cytotoxin (vacA) -- 6.3.1 Geographic Differences in vacA Genotypes -- 6.4 Induced by Contact with Epithelium (iceA) -- 6.5 Outer Membrane Protein -- 6.5.1 Outer Inflammation Protein (oipA) -- 6.5.2 Duodenal Ulcer Promoting Gene A (dupA) -- 6.5.3 Blood Group A Antigen-Binding Adhesion (babA) -- 6.5.4 HomA and HomB -- 6.6 Conclusion -- References -- 7: Host Factor: Genetic Polymorphism -- 7.1 Introduction -- 7.2 Interleukin-1β -- 7.3 Tumor Necrosis Factor-α -- 7.4 Interleukin-10 -- 7.5 Interleukin-8 -- 7.6 Toll-Like Receptor 4 -- 7.7 Nucleotide-Binding Oligomerization Domain-Like Receptors (NLRs) -- 7.8 Conclusions -- References -- Part III: Diagnosis -- 8: Serology -- 8.1 Introduction -- 8.2 Advantages and Disadvantages of Serological Diagnosis -- 8.3 Serological Diagnosis -- 8.3.1 Bacterial Agglutination, Complement Fixation, and Indirect Immunofluorescence Test (IIF) -- 8.3.2 EIA and ELISA -- 8.3.3 Commercial Serological ELISA Kits Depending on H. pylori Antigen -- 8.3.4 Genedia® H. pylori ELISA and Its Use on Nationwide H. pylori Epidemiological Survey in Korea -- 8.3.5 Genedia® H. pylori ELISA and Its Use on Nationwide H. pylori |