Helicobacter pylori and gastric diseases.
Helicobacter pylori (H. pylori) infection is a pathogenic agent of gastric diseases, but their mechanisms are unclear. Effects of ammonia, tumor necrosis factor (TNF), and anti-Lewis autoantibodies induced after H. pylori infection on the development of gastric diseases were investigated. Ammonia disturbed the collagen metabolism in the ulcer base. Soluble TNF receptors regulate the action of TNF. The involvement of anti-Lewis autoantibodies in the development of peptic ulcer might be unlikely. Moreover, H. pylori-specific IgA in gastric juice and TNFalpha gene polymorphism in persons infected with H. pylori were studied. According to H. pylori-specific IgA titer in gastric juice, persons were divided into two histologically and endoscopically different states of disease. TNFA -857 single nucleotide polymorphism (SNP) may be associated with rugal hyperplastic gastritis and gastric carcinomas without severe atrophy. However, complete elucidation of pathogenic mechanisms of H. pylori-induced gastric diseases requires further research.
Goto
Hidemi
H
Department of Gastroenterology, Nagoya University Graduate School of Medicine, Japan. hgoto@med.nagoya-u.ac.jp
D000641:Ammonia / Q000494:pharmacology; D000818:Animals; D000906:Antibodies / Q000737:chemistry; D016481:Helicobacter Infections; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D007070:Immunoglobulin A / Q000737:chemistry / Q000378:metabolism; D007983:Lewis Blood Group Antigens / Q000276:immunology; D016256:Lewis X Antigen / Q000276:immunology; D010437:Peptic Ulcer; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D013272:Stomach Diseases / Q000382:microbiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000906:Antibodies; D007070:Immunoglobulin A; D007983:Lewis Blood Group Antigens; D016256:Lewis X Antigen; C094162:Lewis Y antigen; D014409:Tumor Necrosis Factor-alpha; D000641:Ammonia