gastritis/protease

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ADAM proteases involved in inflammation are differentially altered in patients with gastritis or ulcer.

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ADAM metallopeptidase domain (ADAM)9, 10 and 17 have α-secretase activity that regulates ectodomain shedding of factors involved in inflammation, cell proliferation, angiogenesis, and wound healing. The secretase activity of ADAM proteins is known to induce an inflammatory response. However, under

Increased mucosal production of monomeric IgA1 but no IgA1 protease activity in Helicobacter pylori gastritis.

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Immunoglobulin A and IgM are subjected to epithelial transport only when they are produced as polymers with incorporated J chain. Immunocytes containing various Ig isotypes and associated J chain in gastric mucosa, as well as IgA-degrading protease activity in Helicobacter pylori cultures, were

Helicobacter pylori-mediated gastritis induces local downregulation of secretory leukocyte protease inhibitor in the antrum.

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Helicobacter pylori-infected subjects exhibited a strong decline in antral secretory leukocyte protease inhibitor (SLPI) levels compared to H. pylori-negative subjects and subjects from whom H. pylori had been eradicated (P = 0.002). This reduction was specific for the antrum, whereas SLPI

Secretory leukocyte protease inhibitor expression in various types of gastritis: a specific role of Helicobacter pylori infection.

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OBJECTIVE Secretory leukocyte protease inhibitor (SLPI) represents a multifunctional protein of the gastrointestinal mucosa exerting antimicrobial and anti-inflammatory effects. SLPI expression is generally induced during inflammation; however, Helicobacter pylori-mediated gastritis is associated

Arrestin domain containing 3 promotes Helicobacter pylori-associated gastritis by regulating protease-activated receptor 1

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Arrestin domain containing 3 (ARRDC3) represents a newly discovered α-arrestin involved in obesity, inflammation and cancer. Here we demonstrated a pro-inflammation role of ARRDC3 in H. pylori-associated gastritis. Increased ARRDC3 was detected in gastric mucosa of patients and mice infected with H.

Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5.

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Chronic gastritis from Helicobacter pylori infection is a major factor in the development of gastric adenocarcinoma. Factors that regulate gastritis severity are important in determining which individuals are susceptible to H. pylori-associated disease. Although protease-activated receptor 1 (PAR1)

Number, fixation properties, dye-binding and protease expression of duodenal mast cells: comparisons between healthy subjects and patients with gastritis or Crohn's disease.

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There is an accumulation of evidence to suggest that mast cells may play a key role in gastrointestinal inflammation. We have investigated the numbers and heterogeneity in staining properties of mast cells in biopsies of the duodenum of normal subjects (n = 10), and of normal duodenum from patients

Polymorphisms in MUC1, MUC2, MUC5B and MUC6 genes are not associated with the risk of chronic atrophic gastritis.

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Mucins represent major components of the mucous layer in the stomach, protecting the underlying epithelium from acid, mechanical trauma, proteases and pathogenic bacteria. Previous studies have shown an association of neoplastic transformation in the stomach with aberrant mucin levels, suggesting a

Relationship between histopathological status of the Helicobacter pylori infected patients and proteases of H. pylori in isolates carrying diverse virulence genotypes.

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Helicobacter pylori is the main cause of several gastroduodenal diseases in Humans. Among various virulence factors of H. pylori, proteases may also be involved in its pathogenicity. In this study, relationship between proteolytic activity of H. pylori strains and histopathological changes of the

Protease-activated receptors: novel central role in modulation of gastric functions.

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Protease-activated receptors (PARs) are members of a subfamily of G-protein-coupled receptors that regulate diverse cell functions in response to proteolytic cleavage of an anchored peptide domain that acts as a 'tethered' receptor-activating ligand. PAR-1 and PAR-2 in particular are present

[Effect of FUT-187, oral serine protease inhibitor, on inflammation in the gastric remnant].

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Excessive enterogastric reflux following partial gastrectomy is believed to be responsible for the cause of inflammation in the gastric remnant. We examined the effect of FUT-187, a synthetic serine protease inhibitor, on symptoms and endoscopic findings in 33 patients who were diagnosed

Protease-activated receptor-1 down-regulates the murine inflammatory and humoral response to Helicobacter pylori.

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OBJECTIVE Helicobacter pylori infection results in a diversity of pathologies, from asymptomatic gastritis to adenocarcinoma. The reason for these diverse outcomes is multifactorial and includes host factors that regulate severity of Helicobacter-induced gastritis. Protease-activated receptors (PAR)

Extensive hemorrhagic erosive gastritis associated with acute pancreatitis successfully treated with a somatostatin analog.

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In massive hemorrhage from acute gastric mucosal lesions, it is occasionally difficult to control the bleeding with nonsurgical therapy. We used the somatostatin analog, octreotide, which suppresses gastric and pancreatic function, to treat severe hemorrhagic erosive gastritis in a patient with

Expression and cytoprotective effect of protease-activated receptor-1 in gastric epithelial cells.

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Thrombin is a serine protease involved in many physiological functions and its receptor. the protease-activated receptor-1 (PAR-1), has a wide tissue distribution. We hypothesized that PAR-1 is expressed in gastric epithelial cells and that thrombin can modulate defence mechanisms through PAR-1. The

Genetic diversity of the Helicobacter pylori haemagglutinin/protease (hap) gene.

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Helicobacter pylori has been associated with the etiology of gastritis, gastric and duodenal ulcers and gastric cancer in man. In this study we confirm the presence of the haemagglutinin/protease (hap) gene in ten geographically diverse strains of H. pylori, but the Southern analysis of genomic DNA

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