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Background: Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) have recently been shown to be important in tissue breakdown and remodeling in gut with inflammatory bowel disease. The role of MMPs and TIMPs remains largely unexplored in Helicobacter pylori-associated gastritis (HAG). The aim of this study was to investigate the expression of these proteolytic enzymes in HAG., Methods: Cell-surface or/and intracellular expression of MMP-2, 7, 9 and MT1-MMP and TIMPs (TIMP-2 and -4) was determined in gastric epithelium and infiltrative mucosal lymphocytes (IML) in single endoscopic biopsies from H. pylori-infected (n = 25) and uninfected (n = 15) patients. The quantitative analysis was based on the percentage of positive cells detected by flow cytometry., Results: Secreted MMPs and TIMPs as well as membrane type 1-MMP were shown to be localized mainly on the cell surface of both epithelial cells and IML in HAG. H. pylori significantly up-regulated the cell-surface expression not only of MMPs, but also of TIMPs on IML within tissues. The expression of these molecules on IML was correlated with the grade of gastritis., Conclusions: MMPs and TIMPs expressed on gastric epithelium and H. pylori-antigen(s)-stimulated IML may be implicated in mucosal degradation and remodeling of the stomach. These might contribute to the pathogenesis and progression of atrophy and intestinal metaplasia of gastric mucosa.

Background: How Helicobacter pylori infection affects gastric acid secretion has not been made clear. This study aimed to elucidate the effects of H. pylori infection on H+/K+-adenosine triphosphatase (ATPase) mRNA in gastric fundic gland mucosa., Methods: Twenty patients with chronic gastritis and H. pylori infection were treated with lansoprazole and antibiotics. Before and 1 month after treatment gastroduodenoscopy was performed, and changes in the amount of H+/K+-ATPase mRNA in the fundic gland mucosa, gastric juice pH, and serum gastrin levels were determined., Results: The amount of H+/ K+-ATPase mRNA in the fundic gland mucosa was increased in patients with eradication of H. pylori, in whom significant decreases in gastric juice pH and serum gastrin levels were observed. No significant changes were observed in patients without eradication of H. pylori., Conclusions: These results suggest that one of the mechanisms by which H. pylori infection suppresses acid secretion is by the inhibition of proton pump synthesis in parietal cells.

Serum lysozyme was reevaluated in inflammatory bowel disease and other gastrointestinal disorders. A total of 109 patients were divided into six groups: ulcerative colitis (28), Crohn's disease (9), simple atrophic gastritis (16), atrophic gastritis and pernicious anemia (23), functional dyspepsia (17), and controls (16). Elevated levels of lysozyme, compared with control levels, were found not only in ulcerative colitis and Crohn's disease but also in atrophic gastritis with or without pernicious anemia and in functional dyspepsia. The elevation of lysozyme, since it results from the product of granulocytes and macrophages present in increased amounts in the mucosa of inflammatory bowel diseases, is easily explained. The cellular infiltration in atrophic gastritis may also explain the elevated lysozyme levels. The higher lysozyme levels in some patients with functional dyspepsia could possibly reflect an underlying latent inflammatory process.

Flow cytometric measurements of cellular DNA have been performed on biopsy specimens obtained by gastroscopy in patients with normal gastric mucosa (controls), superficial and atrophic gastritis, and resected stomachs. Aneuploidy was found in two biopsy specimens from a patient with superficial gastritis and in one specimen from a resected stomach. The fractional number of cells with a DNA content corresponding to the DNA synthetic and (G2 + M) phases of the cell cycle was defined as the 'proliferative index' (PI). No difference between the antral and body part of the stomach was found for the PI in controls or between controls and superficial and atrophic gastritis. PI was weakly but significantly correlated to a selection of mucosal enzymes. In resected stomachs increased PI was found when compared with that in the body part of the stomach in controls (p less than 0.01). Biopsy specimens with intestinal metaplasia (p less than 0.01) or atrophy (p less than 0.05) in the resected stomach showed significantly higher PI when compared with specimens with such findings from the body part of the stomach in atrophic gastritis.

Biopsy specimens from the antral and body part of the stomach were studied for a range of marker enzymes in 11 patients with superficial gastritis, 9 patients with atrophic gastritis, and 31 Billroth-II-resected patients and compared with activities found in controls with normal gastric mucosa. In the antral part of the stomach increased gamma-glutamyltransferase activity was found in superficial (p less than 0.01) and atrophic gastritis (p less than 0.05), whereas monoamine oxidase activity was decreased in superficial (p less than 0.01) and atrophic gastritis (p less than 0.05). In the body part, increased activity of gamma-glutamyltransferase (p less than 0.01) and acid-beta-glucuronidase (p less than 0.01) was found in superficial gastritis. In atrophic gastritis increased activities for lactase (p less than 0.01), alkaline phosphatase (p less than 0.05), leucyl-beta-naphthylamidase (p less than 0.05), gamma-glutamyltransferase (p less than 0.05), 5'-nucleotidase (p less than 0.01), N-acetyl-beta-D-glucosaminidase (p less than 0.05), and acid-beta-glucuronidase (p less than 0.01) were found. Specimens from the gastric remnant showed an enzyme activity pattern similar to that seen in the body in atrophic gastritis, apart from a significantly decreased monoamine oxidase activity (p less than 0.004). Specimens with dysplasia in the gastric remnant showed decreased monoamine oxidase activity when compared with specimens without dysplasia (p less than 0.01).