T-bet expression and IFN-γ production

increased, while ST

T-bet expression and IFN-γ production

increased, while STAT6 activation and IL-4 production decreased following therapy with celecoxib and celecoxib plus lansoprazole, respectively. Th1 and Th2 signaling pathways down-regulated after therapy with lansoprazole, and this was associated with an improvement of gastritis. Effect of therapy was not affected by H. pylori status. Conclusion:  Celecoxib and lansoprazole modulate Th1/Th2 immune response in human gastric mucosa. The use of these drugs KU-57788 chemical structure may interfere with long-term course of gastritis. “
“It has previously been reported that weak serum IgG but elevated IgA antibody responses against H. pylori may be associated with risk of gastric cancer (GC) development. To search for potential immunologic markers for GC, we analyzed antibody responses against H. pylori in risk groups of cancer mTOR inhibitor development. Sera and stomach biopsies collected from H. pylori-infected GC patients as well as from patients with gastric ulcer (GU), atrophic gastritis, intestinal metaplasia (IM) and duodenal ulcer and from H. pylori-infected control subjects without atrophy or IM, and in addition from H. pylori-negative subjects

were analyzed for IgG and IgA antibodies against three different H. pylori antigen preparations, that is, membrane protein (MP), urease, and CagA. We observed an increased serum IgA/IgG titer ratio against H. pylori anti-MP in GC and GU patients, and against CagA in Hp-infected GC patients and risk groups. Female patients with GC had a higher serum anti-MP IgA/IgG titer ratio and a higher proportion of poorly differentiated cancer compared with male patients. As earlier observed, the non-tumorous mucosa of H. pylori-infected GC patients contained considerably lower levels of total IgA and H. pylori-specific

IgA compared with H. pylori-infected controls. Similarly, we observed decreased specific mucosal anti-MP IgA response in patients with IM. We observed several differences in local and systemic immunologic responses against H. pylori in H. pylori-infected GC patients and putative GC risk group patients compared with H. pylori-infected controls. These findings may be of importance in efforts to identify risk groups of GC or early stages of GC. “
“Background:  MCE “Candidatus Helicobacter heilmannii” induce chronic gastritis, which eventually leads to gastric B-cell type mucosa-associated lymphoid tissue (MALT) lymphoma. This study was performed using an animal model of infection with “Candidatus Helicobacter heilmannii” to elucidate how this chronic inflammation is induced or maintained. Materials and Methods:  BALB/c mice were infected with the “Candidatus Helicobacter heilmannii” isolate SH4. The animals were examined at 8, 26, 54, and 83 weeks after the infection. The stomach of the animals was resected and immunostained for peripheral lymph node addressin (PNAd) and mucosal addressin cell adhesion molecule 1 (MAdCAM-1), “Candidatus Helicobacter heilmannii,” and CD45R/B220.

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