title: [Molecular-pathological analysis of Helicobacter pylori-associated disorders and clinical laboratory testing].
abstract: Helicobacter pylori (H. pylori) infection causes gastro-duodenal diseases and a wide variety of non gastrointestinal tract conditions, such as idiopathic thrombocytopenic purpura (ITP). Many reports have provided robust evidence for understanding the pathogenesis of H. pylori. However, its cell division process is little known. H. pylori exhibits marked genetic diversity to survive under various stress conditions, leading to the emergence of a variety of clones with novel characteristics. In this report, we briefly summarize our results. H. pylori urease is essential to live in a low-pH environment. Bacterial motility and urea taxisis are also important features for persistent infection. The urease is controlled in response to the pH via post translational regulation. Genetic rearrangement occurs during persistent infection of an individual's stomach, which results in the appearance of a variety of new strains with novel characteristics. The cdrA (cell division-related gene A)--dysfunctional strain had acquired such novel characteristics: increased viability, long-term survival, and tolerance to antibiotics. Furthermore, colonization by a cdrA-dysfunctional strain results in decreased IL-8 production and, hence, attenuates the host's immunity to cause persistent infection. Among the factors involved in the bacterium-host interaction and pathogenesis, we describe the H. pylori CagA, BabA, SabA, and SOD. We discovered two H. pylori phages, including a new type of spherical phage, which cannot be classified into any existing virus category. The phages probably contribute to the evolution and pathogenesis of H. pylori. Eradication therapy covered by health insurance was approved for H. pylori-associated ITP. We reported an extra mechanism, the immunocomplex model (platelets, bacterial molecules, and anti H. pylori antibodies), in the development of H. pylori associated ITP. On the other hand, increased cases of unsuccessful eradication therapy are due to the increased occurrence of drug-resistant H. pylori. Non-antibiotic substances with anti-H. pylori activity are attracting much attention.
authors: Hiroaki
authors: H
authors: Takeuchi
authors: Norihito
authors: N
authors: Morimoto
authors: Tetsuro
authors: T
authors: Sugiura
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000276:immunology / Q000378:metabolism / Q000627:therapeutic use*; D000907:Antibodies, Bacterial / Q000276:immunology / Q000378:metabolism / Q000627:therapeutic use*; D000942:Antigens, Bacterial / Q000235:genetics / Q000276:immunology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000276:immunology / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology
chemical_list: D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial