Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.5 (urease)
 7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well known that abnormal immune responses may play a pathogenic role in the H. pylori-related gastropathy. Indeed, as far as humoral immune response is concerned, it is still debated whether specific anti-H. pylori antibodies have a protective or noxious effect in infected hosts. Besides proinflammatory cytokines released from macrophages, such as tumor-necrosis factor-a and interleukin-1beta, and IFN-gamma derived from T-helper 1 lymphocytes, also interleukin-10, a product of T-helper 2 lymphocytes with antiinflammatory properties, seems to be surprisingly involved in the pathogenesis of H. pylori-induced gastritis. In addition, lipopolysaccharide derived from the outher membrane of H. pylori acts as a chemoattractant for monocytes and induces release of free radicals, interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha. On the other hand, H. pylori lipopolysaccharide could be responsible for the increased polyamine concentrations in the gastric mucosa and polyamines, such as putrescine, spermidine and spermine, could be involved in the increased cell proliferation and consequent possible neoplastic transformation of the gastric mucosa. Incubation of peripheral blood mononuclear cells with H. pylori increases significantly the surface expression of CD95 receptor (Fas), thus suggesting that these bacteria are able to induce apoptosis. In animal models, different types of vaccination have been investigated, including stimulation of nasal and rectal lymphoid tissue, as well as adoptive transfer of T cell from donors immunized with H. pylori. However, results obtained are frequently disappointing. In humans, urease of H. pylori was safely used as oral vaccine in the absence or presence of adjuvants with encouraging results. Finally, DNA vaccines could offer in the future advantages for prophylactic H. pylori eradication, especially where population is infected by this microorganism since childhood.
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PMID:Helicobacter pylori infection, immune response and vaccination. 1247 86

Helicobacter pylori is a spiral, gram-negative rod-shaped pathogen that attaches to gastric epithelial cells in the human stomach and is a causative agent of chronic active gastritis, peptic ulcer and neoplasia. H. pylori is one of the most common pathogens afflicting humans and is the major environmental factor in the development of gastric cancer increasing from 4 to 6 folds the risk of its development. Several specific virulence factors are implicated in the mechanism of H. pylori infection like the bacterial motility; the secretion of large amounts of urease; specific adhesins for the interaction between H. pylori and the gastric surface epithelium; the traslocation into gastric ephitelial cells of the cytotoxin-associated gene A (CagA), the vacuolating cytotoxin A (VacA) and the heat shock protein HspB. Adherence of H. pylori to the gastric epithelium and secretion of interleukins are believed to be an important step in the induction of active inflammation of the mucosal layer. Several studies have demonstrated that H. pylori infection induces gastric epithelial cell proliferation activating ERK and MAPK pathways and increase of mitosis and mutations. Therefore, H. pylori infection seems to increase apoptosis, implying increased gastric epithelial cell turnover. Recently, it has been shown that H. pylori-induced apoptosis in gastric epithelial cells is mediated via the CD95-receptor/ ligand system but that TRAIL also plays an important role in this regulation.
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PMID:Helicobacter pylori and gastric epithelial cells: from gastritis to cancer. 1627 May 19