Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is thought that Helicobacter pylori colonization of the gastric mucosa might stimulate the production of several cytokines, which might trigger and maintain the gastric inflammation associated with Helicobacter pylori infection. In the present study we evaluated interleukin-1 beta. interleukin-6, and the soluble receptor of interleukin-2 both in mucosal homogenates and in the sera of Helicobacter pylori-infected (39 cases) and uninfected (40 cases) patients to investigate whether there was any relationship between variations in cytokines and (1) the severity of Helicobacter pylori-associated gastritis or (2) CagA-positive Helicobacter pylori strains. Mucosal, but not serum levels of interleukins-1 and -6 and interleukin-2 receptor were significantly higher in infected than uninfected patients. Serum levels of Helicobacter pylori antibodies were significantly higher in infected than uninfected patients. These levels correlated with mucosal interleukin-1 beta. The degree of antral or body inflammatory grade was higher in infected than in uninfected patients; cytokines levels were higher in patients with high-grade gastritis, most of whom were Helicobacter pylori positive. Patients infected with CagA-positive strains also had higher levels of interleukin-1 beta, but not of interleukin-2 receptor or interleukin-6. In conclusion. Helicobacter pylori infection results in a local increase in interleukins-1 beta and -6 and interleukin-2 receptor associated with high-grade mucosal inflammation. Interleukin-1 beta seems to favor anti-Helicobacter pylori antibody production, and mucosal levels are enhanced mainly in patients infected with cytotoxic Helicobacter pylori strains.
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PMID:Helicobacter pylori infection enhances mucosal interleukin-1 beta, interleukin-6, and the soluble receptor of interleukin-2. 890 54

Patients with Helicobacter pylori-associated gastritis have an increased release of gastrin. The mechanisms by which H. pylori affects the endocrine cells are unclear. We have used primary cultures containing canine antral G cells to examine the effects of human blood mononuclear cells, purified monocytes and lymphocytes, recombinant cytokines, and NH4Cl on gastrin release. Mononuclear cells and purified monocytes in direct contact with G cells stimulated gastrin release dose dependently. Separating mononuclear cells from G cells by Transwell filters with 0.4-micron pore size still produced a significant increase of gastrin release. Three human recombinant cytokines, interferon-gamma, tumor necrosis factor-alpha, and interleukin-2, but not interleukin-6 and interleukin-1 beta, each produced dose-dependent increases of gastrin stimulation. NH4Cl did not stimulate gastrin release. We conclude that mononuclear cells and purified monocytes prepared from human blood, as well as several cytokines, stimulate gastrin release from antral G cells. These factors may play an important role in the pathogenesis of H. pylori-associated hypergastrinemia.
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PMID:Mononuclear cells and cytokines stimulate gastrin release from canine antral cells in primary culture. 896 89