Antigastric autoantibodies in Helicobacter pyloriinfection: implications of histological and clinical parameters of gastritis

Abstract

Background-It has recently been shown that humoral antigastric autoreactivities occur in a substantial number of Helicobacter pylori infected patients. Aims-To analyse the relevance of such antigastric autoantibodies for histological and serological parameters of the infection as well as for the clinical course. Methods-Gastric biopsy samples and sera from 126 patients with upper abdominal complaints were investigated for evidence of H pylori infection using histology and serology. Autoantibodies against epitopes in human gastric mucosa were detected by immunohistochemical techniques. Histological and clinical findings of all patients were then correlated with the detection of antigastric autoantibodies. Results-H pylori infection was significantly associated with antigastric autoantibodies reactive with the luminal membrane of the foveolar epithelium and with canalicular structures within parietal cells. The presence of the latter autoantibodies was significantly correlated with the severity of body gastritis, gastric mucosa atrophy, elevated fasting gastrin concentrations, and a decreased ratio of serum pepsinogen I:II. Furthermore the presence of anticanalicular autoantibodies was associated with a greater than twofold reduced prevalence for duodenal ulcer. Conclusion-The data indicate that antigastric autoantibodies play a role in the pathogenesis and outcome of H pylori gastritis, in particular in the development of gastric mucosal atrophy. (Gut 1997; 41: 619-623)

Gastric Parietal Cell Antibodies, Helicobacter Pylori Infection, and Chronic Atrophic Gastritis: Evidence from a Large Population-based Study in Germany

“…However, conflicting results have also been reported (24,29). Simultaneous occurrence of H. pylori infection and autoimmune reaction observed in previous investigations (5)(6)(7)(8) or our study population cannot be interpreted to support a causal relationship between bacterial infection and autoimmune response. Because of the crosssectional study design with simultaneous ascertainment of infection, autoimmune response and CAG, temporal relationships between occurrence of bacterial infection, autoimmune response and development of CAG as well as potential disease-related loss of H. pylori infection could not be observed.…”

“…Following the discovery of Helicobacter pylori (H. pylori) and the establishment of a causal relationship between H. pylori infection and CAG (1,2), several studies have reported that a considerable number of patients with H. pylori infection also expressed autoantibodies against Hþ/Kþ-ATPase (5)(6)(7)(8). The presence of these autoantibodies in H. pylori infection was also significantly associated with higher fasting serum gastrin levels, a lower pepsinogen I to II ratio, and reduced secretion of gastric acid (8)(9)(10). In addition, pernicious anemia, which was earlier considered as an exclusive complication of autoimmune gastritis (11), was also shown to be accompanied by H. pylori infection (12)(13)(14).…”

Generation and Characterization of Human Monoclonal scFv Antibodies against Helicobacter pylori Antigens

“…Microtiter plates (Nunc) were coated with antigen in coating buffer (0.2 M Na 2 CO 3-NaHCO 3 [pH 9.6]) at a concentration of 1 g per well by an overnight incubation at 4°C. After three washes with PBS, 10 11 phages (or 100 l of bacterial supernatant) per well were added and incubated for 2 h at RT. Binding of the phage particles to antigen was detected with the anti-M13 antibody B62-FE2 (Progen, Heidelberg, Germany), a mouse monoclonal antibody specific for the major coat protein pVIII, 10% (vol/vol) in M-PBS.…”

“…Furthermore, about 30% of H. pylori-infected patients develop autoantibodies that are reactive with human gastric antigens, such as the H ϩ ,K ϩ -ATPase. This H. pyloriassociated antigastric autoimmunity has been shown to correlate with atrophy of gastric mucosa (6,10,24). Therefore, further analysis of the humoral immune response following H. pylori infection might give new insight into the pathogenesis of H. pylori gastritis.…”

A Novel Proliferation-Associated Variant of CFR-1 Defined by a Human Monoclonal Antibody

“…In addition to the cellular changes induced by the H. pylori proteins, it has become clear in recent years that the bacterial infection and the development of gastritis and stomach cancer are accompanied by autoimmunity Faller et al, 1997), which may also lead to degenerative processes of the stomach mucosa (Negrini et al, 1991).…”