Antigastric autoantibodies in Helicobacter pylori gastritis: prevalence, in-situ binding sites and clues for clinical relevance

Abstract

Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.

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.…”

“…3,4). 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).…”

Epithelial attachment alters the outcome of Helicobacter pylori infection

“…Parietal cell autoantibodies have been correlated with the occurance of atrophic gastritis in H. pylori infected humans (21,22). To screen for autoantibodies, sera from infected transgenic and normal mice were incubated with sections prepared (Fig.…”

Characterization of the Gastric Immune Response in Cheetahs (Acinonyx jubatus) WithHelicobacter-Associated Gastritis

“…32 In addition to the cellular immune response, the humoral response to H. pylori may contribute to disease pathogenesis. 14,15,43 Approximately 89% of H. pylori-infected humans develop anti-Helicobacter antibodies that cross-react with the gastric mucosa, 41 and 25% of these individuals develop antibodies that bind to the canaliculi of parietal cells. 6 These autoantibodies have been correlated with the presence and degree of inflammation and with atrophy of the gastric glands.…”

“…43 Specifically, the binding of antibodies to parietal cell canaliculi was significantly correlated with H. pylori infection, the presence of fundic (and not antral) gastritis, increased numbers of periglandular and IELs, increased destruction of the fundic glands, and gastric atrophy. [14][15][16]42,43,51 This histologic pattern is most similar to that commonly seen in captive cheetahs, so it is possible that affected cheetahs may also develop Helicobacter antibodies that cross-react with the gastric epithelium.…”