The story so far: Helicobacter pylori and gastric autoimmunity (original) (raw)
Related papers
Autoantibodies to Gastric Mucosa in Helicobacter pylori Infection
Helicobacter, 1997
Background.Although Helicobacter pylori is recognized as the main cause of chronic gastritis and its associated diseases, very little is known about the pathogenetic mechanisms leading to intestinal metaplasia and atrophic gastritis.Methods.We reviewed the data regarding the possible pathogenetic role played by the anti–H. pylori immune responses in the genesis of atrophic gastritis and intestinal metaplasia.Results.Although only type A (corpus‐restricted atrophic gastritis), often associated to pernicious anemia, is considered autoimmune in nature, abundant evidence supports the presence of cellular and humoral autoimmune responses also in patients with H. pylori infection. In a mechanism known as antigenic mimicry, highly conserved immunogenic molecules expressed by infectious pathogens may act as a trigger for the induction of humoral and cellular immune responses that cross‐react with host cellular antigens. Numerous studies support the view that H. pylori is very effective in i...
Mucosal Production of Antigastric Autoantibodies in Helicobacter pylori Gastritis
Helicobacter, 2001
Background. Apart form bacterial virulence factors of Helicobacter pylori , certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the development of gastric atrophy. The aim of this study was to analyze the possible antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e., in the gastric mucosa. Material and Methods. Gastric biopsy specimens from antrum and corpus mucosa of 24 H. pylori-infected and of 33 noninfected patients were cultured for 3 days, and tissue culture supernatants were analyzed for the amount of locally produced IgA and IgG. Antigastric autoantibodies were screened in the sera and in the su-pernatants by means of immunohistochemistry. Results. The infected patients had significantly higher concentrations of locally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodies, or both, were detectable only in the sera (38%) and supernatants (17%) of infected patients. Interestingly, the patient with the strongest local autoimmune response showed body-predominant H. pylori gastritis, with destruction of gastric glands and atrophy of the body mucosa. Conclusions. These results demonstrate that antigastric autoimmune reactions are detectable at the site of the disease and might be relevant for the pathogenesis of gastric mucosa atrophy in H. pylori gastritis.
Association of Helicobacter pylori and gastric autoimmunity: A population-based study
FEMS Immunology and Medical Microbiology, 1995
Based on clinical studies, a negative association between Helicobacter pylori and autoimmune corpus gastritis is described. In the present investigation of an unselected population of 1461 adults we can state, however, that there exists a relationship between H. pylori infection and the development of gastric corpus autoimmunity. As confirmation for the gastric autoantibody development through molecular mimicry, a high homology (72% in 25 amino acid overlap) between the beta subunit of H. pylori urease and that of H + K + ATPase, the gastric parietal cell autoantigen, was revealed.
Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection
2010
To study the association between Helicobacter pylori (H. pylori ) infection and autoimmune type atrophic gastritis. METHODS: Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology, immunoblot-based serology, and histology to reveal a past or a present H. pylori infection. In addition, serum markers for gastric atrophy (pepsinogen Ⅰ, pepsinogen Ⅰ/Ⅱ and gastrin) and autoimmunity [parietal cell antibodies (PCA), and intrinsic factor (IF), antibodies] were determined.
Gastroenterology, 1998
Background & Aims: A subgroup of Helicobacter pyloriinfected patients develops autoantibodies to gastric parietal cell canaliculi. The aim of this study was to define the unknown autoantigen. Methods: We screened 72 H. pylori-infected patients, 5 patients with autoimmune gastritis, and 36 healthy controls for immunoglobulin G autoantibodies to canaliculi by immunohistochemistry. The antigen specificity was determined by immunoprecipitation of the murine gastric H ؉ ,K ؉-adenosine triphosphatase (H ؉ ,K ؉-ATPase) expressed in oocytes and by immunoblotting on human gastric membranes from the body mucosa. Results: Autoantibodies specific for the conformational peptides of the H ؉ ,K ؉-ATPase were detected in 3% (1/36) of controls, in all patients with autoimmune gastritis (5/5), in 25% (18/72) of H. pylori-infected patients, and in 47% (15/32) of the infected patients with anticanalicular autoantibodies. No other major autoantigen was identified. Atrophy in the gastric body mucosa was found in 60% (9/15) of infected patients with both anticanalicular and anti-H ؉ ,K ؉-ATPase antibodies, but only in 13% (5/37) of infected patients lacking both autoantibodies (P F 0.01). Conclusions: The gastric H ؉ ,K ؉-ATPase is a major autoantigen in H. pyloriassociated antigastric autoimmunity. Thus, anti-H ؉ ,K ؉-ATPase autoantibodies, which are closely linked to classical autoimmune gastritis, are also significant indicators for body mucosa atrophy in chronic H. pylori gastritis.
Gut, 1997
Background—It has recently been shown that humoral antigastric autoreactivities occur in a substantial number ofHelicobacter 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 se...
Helicobacter pylori , T cells and cytokines: the âdangerous liaisonsâ
FEMS Immunology & Medical Microbiology, 2005
Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-c, TNF-a, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin-and Fas-Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H + K + ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry.