Abstract
Atrophic autoimmune gastritis (AAG) is a condition of chronic inflammation and atrophy of stomach mucosa, for which development can be partially triggered by the bacterial pathogen Helicobacter pylori (HP). HP can cause a variety of gastric diseases, such as duodenal ulcer (DU) or gastric cancer (GC). In this study, a comparative proteomic approach was used by two-dimensional fluorescence difference gel electrophoresis (DIGE) to identify differentially expressed proteins of HP strains isolated from patients with AAG, to identify markers of HP strain associated with AAG. Proteome profiles of HP isolated from GC or DU were used as a reference to compare proteomic levels. Proteomics analyses revealed 27 differentially expressed spots in AAG-associated HP in comparison with GC, whereas only 9 differential spots were found in AAG-associated HP profiles compared with DU. Proteins were identified after matrix-assisted laser desorption ionization (MALDI)-TOF and peptide mass fingerprinting. Some AAG-HP differential proteins were common between DU- and GC-HP (peroxiredoxin, heat shock protein 70 [HSP70], adenosine 5'-triphosphate [ATP] synthase subunit α, flagellin A). Our results presented here may suggest that comparative proteomes of HP isolated from AAG and DU share more common protein expression than GC and provide subsets of putative AAG-specific upregulated or downregulated proteins that could be proposed as putative markers of AAG-associated HP. Other comparative studies by two-dimensional maps integrated with functional genomics of candidate proteins will undoubtedly contribute to better decipher the biology of AAG-associated HP strains.
Highlights
Autoimmune gastritis (AG), known as autoimmune chronic atrophic gastritis or chronic type A gastritis, is an autosomal-dominant disease
In the Helicobacter pylori (HP) strains successfully isolated from biopsies of four atrophic AG (AAG) patients (Table 1), we hereby used difference gel electrophoresis (DIGE) to identify differentially expressed proteins, compared with those isolated from duodenal ulcer (DU) and gastric cancer (GC) biopsies
Protein spot maps from antrum and corpus of the same patient analyzed with principal component analysis (PCA) were close and not different; independently from the patient, within each group (AAG, GC or DU), spot maps from corpus and antro were not placed in distinct subgroups
Summary
Autoimmune gastritis (AG), known as autoimmune chronic atrophic gastritis or chronic type A gastritis, is an autosomal-dominant disease. AG is characterized by immune-mediated chronic inflammation, mucosal gland atrophy, with increased serum autoantibodies to gastric parietal cells and/or intrinsic factors, hypochlorhydria, vitamin B12 deficiency and, in some cases, neurological symptoms and diffuse metaplasia. In the presence of atrophy, AG is called atrophic AG (AAG). In Correa’s model of gastric carcinogenesis, Helicobacter pylori (HP) infection triggers the progressive sequence of gastric lesions from chronic gastritis, gastric atrophy, intestinal metaplasia, dysplasia and gastric adenocarcinoma [5]. Metaplastic AAG demonstrates similar histological and clinical findings as those of metaplastic AG related to HP [3]. In the early phases of AG, HP infection may induce autoantibodies to gas-
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