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Human Gastric Mucosa (human + gastric_mucosa)

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Medical Sciences	100%

Selected Abstracts

Natural Killer Cell Receptor+ T-Lymphocytes in Normal and Helicobacter pylori -Infected Human Gastric Mucosa

HELICOBACTER, Issue 6 2008
Joan O'Keeffe
Abstract Background:,Helicobacter pylori infection is associated with development of chronic inflammation and infiltration of immune cells into the gastric mucosa. As unconventional T-lymphocytes expressing natural killer cell receptors are considered to play central roles in the immune response against infection, a study investigating their frequencies in normal and H. pylori -infected gastric mucosa was undertaken. Materials and Methods:, Flow cytometry was used to quantify T-cells expressing the natural killer cell markers CD161, CD56, and CD94 in freshly isolated lymphocytes from the epithelial and lamina propria layers of gastric mucosa. Thirteen H. pylori -positive and 24 H. pylori -negative individuals were studied. Results:, CD94+ T-cells were the most abundant (up to 40%) natural killer receptor-positive T-cell population in epithelial and lamina propria layers of H. pylori -negative gastric mucosa. CD161+ T-cells accounted for about one-third of all T-cells in both compartments, but the lowest proportion were of CD56+ T-cells. Compared with H. pylori -negative mucosa, in H. pylori -infected mucosa the numbers of CD161+ T-cells were significantly greater (p = .04) in the epithelium, whereas the numbers of CD56+ T-cells were lower (p = .01) in the lamina propria. A minor population (< 2%) of T-cells in both mucosal layers of H. pylori -negative subjects were natural killer T-cells, and whose proportions were not significantly different (p > .05) to those in H. pylori -infected individuals. Conclusions:, The predominance, heterogeneity, and distribution of natural killer cell receptor-positive T-cells at different locations within the gastric mucosa reflects a potential functional role during H. pylori infection and warrants further investigation. [source]

Helicobacter pylori Stimulates a Mixed Adaptive Immune Response with a Strong T-Regulatory Component in Human Gastric Mucosa

HELICOBACTER, Issue 3 2007
Rasmus Goll
Abstract Background:, Host factors play an important role in the pathophysiology of Helicobacter pylori infection and development of gastritis and related disease. The established opinion is that the T-cell-mediated immune response to H. pylori infection is of Th1 type. Our earlier immune cell phenotype studies indicate a mixed Th1,Th2 profile of the effector cells. Therefore, an extensive adaptive and regulatory cytokine gene expression profile was conducted by quantitative real-time polymerase chain reaction (qPCR). Materials and Methods:, Biopsies from gastric mucosa of 91 patients diagnosed as H. pylori negative, H. pylori positive with gastritis, or H. pylori positive with peptic ulcer were obtained by endoscopy. Gene expressions of nine cytokines and CagA status were measured by qPCR. Results:, All cytokine genes showed higher expression levels in the presence of H. pylori when compared to H. pylori- negative samples (fold increase: IL8: × 11.2; IL12A: × 2.4; TNF-,: × 5.2; IFN-,: × 4.3; IL4: × 3.6; IL6: × 14.7; and IL10: × 6.7). Patients infected with CagA-positive strains had higher expression of IL1-, and IL18 compared to patients infected with CagA-negative strains (× 1.6 for IL1-, and × 2.0 for IL18). Patients with duodenal ulcer had a lower antral Th1/Th2 ratio than other H. pylori -positive patients. Conclusions:, The cytokine profile of H. pylori -infected gastric mucosa shows a mixed Th1,Th2 profile. Furthermore, a high IL10 expression may indicate that also regulatory T cells play a role in the chronic phase of H. pylori infection. [source]

Enhanced Activation of Cyclooxygenase-2 Downregulates Th1 Signaling Pathway in Helicobacter pylori -infected Human Gastric Mucosa

HELICOBACTER, Issue 3 2007
Antonia Pellicanò
Abstract Background:, Evidence suggests that an impaired T-cell response against Helicobacter pylori plays a role in the pathogenesis of H. pylori -related diseases. Cyclooxygenase (COX) 2 has been shown to inhibit the production of T-helper (Th) 1 cytokines. This study aimed to ascertain whether COX-2 downregulates Th1 signaling pathway in human gastric mucosa colonized by H. pylori. Methods:, COX-2 expression and prostaglandin E2 (PGE2) production were determined in total proteins extracted from freshly obtained gastric biopsies of H. pylori -infected and uninfected patients by Western blotting and enzyme-linked immunosorbent assay (ELISA). Phosphorylated (p)STAT4, pSTAT1, T-bet, and pSTAT6 expression and interleukin (IL)-12, interferon (IFN)-,, and IL-4 production were also determined by Western blotting and ELISA, respectively, in total protein extracts from gastric biopsy cultures of H. pylori -infected patients treated without and with COX-2 inhibitor NS-398. Results:, Enhanced expression of COX-2 and production of PGE2 was found in H. pylori -infected compared to uninfected patients. COX-2 inhibition significantly increased expression of Th1 transcription factors along with production of IL-12 and IFN-,. By contrast, no changes in the expression of STAT6 and production of IL-4 were found. Conclusion:, This study provides a mechanism by which H. pylori may actually interfere with normal T-cell activation in human gastric mucosa, possibly enhancing its pathogenicity. The use of COX-2 selective inhibitors as immunomodulators in the course of H. pylori infection deserves investigations. [source]

Overexpression of Human Telomerase RNA in Helicobacter pylori -infected Human Gastric Mucosa

CANCER SCIENCE, Issue 11 2000
Kwon Hur
Telomerase, an enzyme associated with cellular immortality and malignancy, plays an important role in cellular immortalization and tumorigenesis. Furthermore, overexpression of the RNA component of the telomerase, called human telomerase RNA (hTR), has been demonstrated in various human cancers as an early event. The pattern of hTR expression following Helicobacter pylori (H. pylori) infection in human gastric mucosa was investigated by a radioactive in situ hybridization (ISH) assay. Paraffin-embedded sections of 50 biopsy specimens taken from the gastric antrum of individual patients infected to different extents with H. pylori, as well as normal gastric mucosa, were studied. In normal gastric mucosa, only weak hTR expression was noted and the expression was limited to basal cells of the gastric glands. However, the degree of hTR expression gradually increased in parallel with the degree of H. pylori infection. The mean scores of gastric mucosa with mild, moderate and severe degrees of H. pylori infection were 2.3, 2.8, and 3.7 times higher than that of normal gastric mucosa, respectively. The results of this study suggested that up-regulation of hTR expression is a frequent and early event associated with H. pylori infection in the gastric mucosa and may play some role in gastric carcinogenesis. Sufficient synthesis of hTR during this early stage may be a prerequisite for telomerase reactivation to occur in gastric cancer. [source]

Naturally Occurring Regulatory T cells (CD4+, CD25high, FOXP3+) in the Antrum and Cardia are Associated with Higher H. pylori Colonization and Increased Gene Expression of TGF-,1

HELICOBACTER, Issue 4 2008
Arne Kandulski
Abstract Background:Helicobacter pylori causes gastric inflammation. Despite the induction of H. pylori -specific B- and T cells, the immune response is not sufficient to clear the infection. Regulatory T cells (Treg cells) suppress the activation and proliferation of antigen-specific T cells and mediate immunologic tolerance. FOXP3 was shown to be expressed in a subset of Treg cells known as ,naturally occurring Treg cells'. These cells have not been sufficiently studied in context to H. pylori -induced inflammation in human gastric mucosa. Materials and methods: The study included 76 patients stratified according to the presence of H. pylori. Gene expression levels of FOXP3, transforming growth factor (TGF)-,1, and interleukin-10 were analyzed by quantitative real-time polymerase chain reaction in biopsies from gastric antrum, corpus, and cardia. FOXP3 expression was also analyzed by immunohistochemistry. Differences in expression levels were analyzed by comprehensive statistical analyses and correlated with clinical and histomorphologic parameters. Results:H. pylori -positive patients revealed a 19- to 25-fold induction of FOXP3 transcript levels in antrum and cardia (p < .02). FOXP3 transcript levels correlated positively with inflammation (p < .04) and TGF-,1 transcript levels (p < .001). Furthermore, a positive correlation between FOXP3+ Treg cells and H. pylori colonization was demonstrated. Conclusion: This study demonstrates that H. pylori -induced gastritis is associated with a recruitment of naturally occurring FOXP3+ Treg cells that correlates with the degree of bacterial colonization and mucosal TGF-,1 expression. Together, these data support the hypothesis that naturally FOXP3+ Treg cells play a role in the lifelong persistence of H. pylori infection in humans. [source]

Enhanced Activation of Cyclooxygenase-2 Downregulates Th1 Signaling Pathway in Helicobacter pylori -infected Human Gastric Mucosa

Nutrients Released by Gastric Epithelial Cells Enhance Helicobacter pylori Growth

HELICOBACTER, Issue 6 2004
Karin Van Amsterdam
ABSTRACT Background.,Helicobacter pylori survives and proliferates in the human gastric mucosa. In this niche, H. pylori adheres to the gastric epithelial cells near the tight junctions. In vitro, H. pylori proliferated well in tissue-culture medium near gastric epithelial cells. However, in the absence of epithelial cells, growth of H. pylori could only be established in tissue-culture medium when, prior to the experiment, it was preincubated near gastric epithelial cells. Therefore, we aimed to determine whether diffusion of nutrients derived from epithelial cells was required for H. pylori growth in Dulbecco's modified Eagle's minimal essential medium (DMEM) cell culture medium. Materials and Methods., Cell culture conditions essential for H. pylori growth in vitro were determined with gastric epithelial HM02 cells. Results., Deprivation of iron in cell-culture-conditioned DMEM resulted in a growth arrest of H. pylori. However, near gastric epithelial cells, growth of H. pylori was resistant to iron deprivation. Evidently, when residing close to epithelial cells, H. pylori was able to fulfil its iron requirements, even when the DMEM was deprived of iron. Nevertheless, supplementation with iron alone did not restore H. pylori growth in DMEM, hence other nutrients were deficient as well in the absence of epithelial cells. Growth of H. pylori in DMEM was restored when hypoxanthine, l -alanine and l -proline were added to the DMEM. Conclusions, Diffusion of (precursors of) these nutrients from the gastric epithelial cells is essential for H. pylori growth in vitro. We hypothesize that in vivo, H. pylori favors colonization near the tight junctions, to gain maximal access to the nutrient(s) released by gastric epithelial cells. [source]

Effect of H. pylori on the Expression of TRAIL, FasL and their Receptor Subtypes in Human Gastric Epithelial Cells and their Role in Apoptosis

HELICOBACTER, Issue 5 2004
Jan Hendrik Martin
ABSTRACT Background and Aims., In the human stomach expression of TNF-related apoptosis inducing ligand (TRAIL) and its receptors and the modulatory role of Helicobacter pylori are not well described. Therefore, we investigated the effect of H. pylori on the expression of TRAIL, FasL and their receptors (TRAIL-R1-R4, Fas) in gastric epithelial cells and examined their role in apoptosis. Materials and Methods., mRNA and protein expression of TRAIL, FasL and their receptors were analyzed in human gastric epithelial cells using RT-PCR, Western blot, and immunohistochemistry. Gastric epithelial cells were incubated with FasL, TRAIL and/or H. pylori, and effects on expression, cell viability and epithelial apoptosis were monitored. Apoptosis was analyzed by histone ELISA, DAPI staining and immunohistochemistry. Results., TRAIL, FasL and their receptor subtypes were expressed in human gastric mucosa, gastric epithelial cell primary cultures and gastric cancer cells. TRAIL, FasL and H. pylori caused a time- and concentration-dependent induction of DNA fragmentation in gastric cancer cells with synergistic effects. In addition, H. pylori caused a selective up-regulation of TRAIL, TRAIL-R1 and Fas mRNA and protein expression in gastric cancer cells. Conclusions., Next to FasL and Fas, TRAIL and all of its receptor subtypes are expressed in the human stomach and differentially modulated by H. pylori. TRAIL, FasL and H. pylori show complex interaction mediating apoptosis in human gastric epithelial cells. These findings might be important for the understanding of gastric epithelial cell kinetics in patients with H. pylori infection. [source]

Helicobacter pylori HP1034 (ylxH) is required for motility

HELICOBACTER, Issue 5 2004
Karin Van Amsterdam
ABSTRACT Background.,Helicobacter pylori motility is essential for the colonization and persistence in the human gastric mucosa. So far, more than 50 genes have been described to play a role in flagellar biosynthesis. H. pylori YlxH (HP1034) is annotated as an ATP-binding protein. However, H. pylori YlxH shows similarity to proteins involved in the flagellar biosynthesis of other bacterial species. Moreover, H. pylori ylxH is found adjacent to genes involved in flagellar biosynthesis in the sequenced genomes of H. pylori 26695 and J99. We therefore aimed to determine the role of YlxH in H. pylori motility. Materials and methods., Motility, flagellar biosynthesis and transcriptional regulation of genes encoding flagellar proteins was compared between H. pylori 11A and a knockout of ylxH in H. pylori 11A. Results., The ylxH knockout in H. pylori 11A was nonmotile on soft agar plates, whereas H. pylori 11A was motile. Furthermore, the H. pylori 11A ylxH knockout lacked flagella, while H. pylori 11A possessed two to three flagella. Transcription of H. pylori flaG (HP0751), fliM (HP1031) and fliA (HP1032) was reduced in the H. pylori 11A ylxH¯ knockout, whereas transcription of flaA (HP0601) was not altered. However, Western blot analysis showed substantially reduced amounts of the major flagellin subunit FlaA in the H. pylori 11A ylxH knockout compared to H. pylori 11A. Conclusions.,H. pylori YlxH is essential for the assembly of flagella and hence for the motility of H. pylori. [source]

The Influence of Lactobacillus brevis on Ornithine Decarboxylase Activity and Polyamine Profiles in Helicobacter pylori -Infected Gastric Mucosa

HELICOBACTER, Issue 2 2004
Michele Linsalata
ABSTRACT Background., Functional probiotics may prevent Helicobacter pylori infection, and some evidence suggests that they also possess antitumor properties. Lactobacillus brevis (CD2) is a functional Lactobacillus strain with peculiar biochemical features, essentially related to the activity of arginine deiminase. This enzyme catalyzes the catabolism of arginine and affects the biosynthesis of polyamines (putrescine, spermidine, and spermine). Polyamines are polycations found in high concentrations in both normal and neoplastic cells. Our aims were: 1, to assess whether oral administration of L. brevis (CD2) affects H. pylori survival in the human gastric mucosa; 2, to evaluate the effects of L. brevis (CD2) on polyamine biosynthesis in gastric biopsies from H. pylori- positive patients. Materials and Methods., For 3 weeks before endoscopy, 22 H. pylori- positive dyspeptic patients randomly received (ratio 1 : 1) high oral doses of L. brevis (CD2) or placebo. Before and after treatment, H. pylori infection was determined by urea breath test (UBT). In gastric biopsies, ornithine decarboxylase activity and polyamine levels were, respectively, evaluated by a radiometric technique and high-pressure liquid chromatography (HPLC). Results.,L. brevis (CD2) treatment did not eradicate H. pylori. However, a reduction in the UBT delta values occurred, suggesting a decrease in intragastric bacterial load. Significantly, L. brevis (CD2) induced a decrease in gastric ornithine decarboxylase activity and polyamine levels. Conclusions., Our data support the hypothesis that L. brevis (CD2) treatment decreases H. pylori colonization, thus reducing polyamine biosynthesis. Alternatively, the arginine deiminase activity following L. brevis (CD2) administration might cause arginine deficiency, preventing polyamine generation from gastric cells. [source]

Membrane-bound, ATP-dependent energy systems and tissue hypoxia in human gastric mucosa

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2000
Gyula Mózsik
First page of article [source]

The peptide hormone xenin induces gallbladder contractions in conscious dogs

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2007
Y. Kamiyama
Abstract, Xenin is a 25-amino acid peptide isolated from human gastric mucosa. The biological activities of xenin include modulating intestinal motility and affecting exocrine pancreatic secretion and gastric acid secretion. The physiological effect of xenin on the gastrointestinal tract, however, is incomplete. The objective of this study is to investigate the effects of xenin on the gastrointestinal tract motility of conscious dogs. Gastrointestinal tract and gallbladder contractions were monitored by chronically implanted force transducers. Synthetic xenin was injected intravenously during the interdigestive state with or without pretreatment with cholinergic blockers. The effects of xenin following cholecystectomy and truncal vagotomy were also investigated. Xenin induced gallbladder and jejunal contractions, although a dose-dependent response was shown only with gallbladder contractions. These effects were inhibited by pretreatment with cholinergic blockers, but were not enhanced by truncal vagotomy. The jejunal contractions were completely inhibited by cholecystectomy. The only direct effect of xenin in terms of gastrointestinal motility was to induce gallbladder contractions in conscious dogs. The neural pathway mediating xenin's action was cholinergic, but not the vagal. This novel finding indicates a new role of xenin. [source]

Localization of antigen-presenting cells in Helicobacter pylori -infected gastric mucosa

PATHOLOGY INTERNATIONAL, Issue 4 2002
Tatsuhiko Suzuki
Helicobacter pylori (HP) infection is known to induce the specific immune response in the gastric mucosa. The immune response is triggered by presentation of antigen peptides on the major histocompatibility assembly of the antigen-presenting cells (APC) with the assistance of costimulatory molecules such as B7-1 (CD80) and B7-2 (CD86). Their counter-receptors or ligands on T cells are CD28 or cytotoxic lymphocyte-associated molecule-4. The aim of the present study was to clarify the localization of APC and their relation with T cells in HP-infected human gastric mucosa. Our findings suggest that the macrophages in the lamina propria may mainly act as APC in the HP-infected gastric mucosa, and the triggered immune response might be involved in the mucosal immune response in the inflamed gastric mucosa to invasive antigens related to HP organisms. [source]