SUMMARY
Background:The acid suppressive effect of lansoprazole is influenced by the P450 2C19 (CYP2C19) polymorphism. Aim: To investigate whether the CYP2C19 genotype is related to the healing of erosive reflux oesophagitis during treatment with lansoprazole. Methods: Eighty-eight Japanese patients with erosive reflux oesophagitis were treated with a daily oral dose of 30 mg lansoprazole for 8 weeks. The CYP2C19 genotype, Helicobacter pylori infection status and serum pepsinogen I/II ratio were assessed before treatment. At 4 and 8 weeks, the healing of erosive reflux oesophagitis was evaluated endoscopically. Results: The healing rates were 57.1%, 69.2% and 72.7% at 4 weeks and 77.4%, 95.0% and 100% at
To investigate the role of interferon gamma in the pathogenesis of Crohn's disease, we examined the interferon gamma levels of serum, supernatant of cultured peripheral blood mononuclear cells activated by phytohemagglutinin, and medium of organ culture of colonic mucosa in Crohn's disease. Serum interferon gamma levels in Crohn's disease, especially in active or non-resected Crohn's disease, were more elevated than those in normal subjects. In contrast, the production of interferon gamma by peripheral blood mononuclear cells was reduced in Crohn's disease. In some patients, interferon gamma levels of organ culture medium of colonic mucosal tissue specimens were elevated. When peripheral blood mononuclear cells were preincubated for 72 hours, interferon gamma production in Crohn's disease increased from 23.8% to 62.3% in comparison to levels in healthy controls. These results indicate that elevated serum interferon gamma in Crohn's disease may originate from the intestine, and interferon gamma may be related to the immune reaction and inflammation in the intestine.
Background: Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-3 transmit a same signal needed for growth and activation in granulocytes and macrophages, because these receptors utilize a common beta chain. Little is known about growth factors for intestinal myeloid cells in lesions of inflammatory bowel disease (IBD). Aim: To find out whether GM-CSF is produced by the intestinal cells in IBD patients and controls. Methods: We measured levels of GM-CSF, tumor necrosis factor (TNF), and IL-3 in the media of organ culture and lamina propria mononuclear cells (LPMCs) culture of colonic mucosa from the patients with IBD. Next, we have investigated GM-CSF production of colonic epithelial cell lines. Results: Spontaneous secretion of GM-CSF was increased in inflamed mucosa, while secretion of IL-3 was not detected. Release of GM-CSF was enhanced in LPMCs from inflamed mucosa. Mucosal GM-CSF production was correlated to TNF-α production. Colonic epithelial cell line and T cell produced GM-CSF with superantigen stimulation. Conclusion: We revealed pivotal production of GM-CSF but not IL-3 in intestinal lesion of IBD. Increased secretion of GM-CSF might lead to chronic gut inflammation.
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