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H. Pylori Colonization (h + pylori_colonization)
Selected AbstractsNaturally 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-,1HELICOBACTER, Issue 4 2008Arne 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] Investigation of the Immunomodulatory Effects of Lactobacillus casei and Bifidobacterium lactis on Helicobacter pylori InfectionHELICOBACTER, Issue 3 2008Li Zhang Abstract Background:,Lactobacillus and Bifidobacterium species have shown beneficial effects in the treatment of Helicobacter pylori infection; however, the mechanisms behind such effects are not fully understood. In this study, we have investigated the immunomodulatory effects of probiotics in a mouse model of H. pylori infection. Materials and methods:,H. pylori -infected C57BL/6 mice were treated with L. casei L26, B. lactis B94, or no probiotics for 5 weeks, respectively. Mice not infected with H. pylori were included as normal controls. Gastric histology, protein levels of interleukin (IL)-1,, IL-10, IL-12/23p40, and H. pylori colonization density in the gastric tissues, as well as H. pylori -specific antibodies were examined. Results:, In mice receiving L. casei L26 and B. lactis B94, gastric neutrophil infiltration and IL-1, were significantly decreased and IL-10 was significantly increased as compared with mice receiving no probiotics. In mice receiving B. lactis B94, IL-12/23p40 was significantly increased and H. pylori IgG was significantly reduced as compared with mice receiving no probiotics. No significant difference of H. pylori colonization was observed among the three groups of mice. Conclusion:, The reduced level of IL-1, and neutrophil infiltration observed in mice infected with H. pylori following treatment with L. casei L26 and B. lactis B94 resulted from a modulation of immune response rather than a decrease of H. pylori colonization. Furthermore, B. lactis B94 has the intrinsic ability to promote a Th1 immune response through an increase in IL-12/IL-23. [source] The Influence of Lactobacillus brevis on Ornithine Decarboxylase Activity and Polyamine Profiles in Helicobacter pylori -Infected Gastric MucosaHELICOBACTER, Issue 2 2004Michele 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] High salt diets dose-dependently promote gastric chemical carcinogenesis in Helicobacter pylori -infected Mongolian gerbils associated with a shift in mucin production from glandular to surface mucous cellsINTERNATIONAL JOURNAL OF CANCER, Issue 7 2006Sosuke Kato Abstract Intake of salt and salty food is known as a risk factor for gastric carcinogenesis. To examine the dose-dependence and the mechanisms underlying enhancing effects, Mongolian gerbils were treated with N -methyl- N -nitrosourea (MNU), Helicobacter pylori and food containing various concentrations of salt, and were sacrificed after 50 weeks. Among gerbils treated with MNU and H. pylori, the incidences of glandular stomach cancers were 15% in the normal diet group and 33%, 36% and 63% in the 2.5%, 5% and 10% NaCl diet groups, showing dose-dependent increase (p < 0.01). Intermittent intragastric injection of saturated NaCl solution, in contrast, did not promote gastric carcinogenesis. In gerbils infected with H. pylori, a high salt diet was associated with elevation of anti- H. pylori antibody titers, serum gastrin levels and inflammatory cell infiltration in a dose-dependent fashion. Ten percent NaCl diet upregulated the amount of surface mucous cell mucin (p < 0.05), suitable for H. pylori colonization, despite no increment of MUC5AC mRNA, while H. pylori infection itself had an opposing effect, stimulating transcription of MUC6 and increasing the amount of gland mucous cell mucin (GMCM). High salt diet, in turn, decreased the amount of GMCM, which acts against H. pylori infection. In conclusion, the present study demonstrated dose-dependent enhancing effects of salt in gastric chemical carcinogenesis in H. pylori -infected Mongolian gerbils associated with alteration of the mucous microenvironment. Reduction of salt intake could thus be one of the most important chemopreventive methods for human gastric carcinogenesis. © 2006 Wiley-Liss, Inc. [source] Phytoceuticals: Mighty but ignored weapons against Helicobacter pylori infectionJOURNAL OF DIGESTIVE DISEASES, Issue 3 2008Sun-Young LEE Helicobacter pylori (H. pylori) infection causes peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphomas and gastric adenocarcinomas, for which the pathogenesis of chronic gastric inflammation prevails and provides the pathogenic basis. Since the role of H. pylori infection is promoting carcinogenesis rather than acting as a direct carcinogen, as several publications show, eradication alone cannot be the right answer for preventing H. pylori -associated gastric cancer. Therefore, a non-antimicrobial approach has been suggested to attain microbe-associated cancer prevention through controlling H. pylori -related chronic inflammatory processes and mediators responsible for carcinogenesis. Phytoceutical is a term for plant products that are active on biological systems. Phytoceuticals such as Korean red ginseng, green tea, red wine, flavonoids, broccoli sprouts, garlic, probiotics and flavonoids are known to inhibit H. pylori colonization, decrease gastric inflammation by inhibiting cytokine and chemokine release, and repress precancerous changes by inhibiting nuclear factor-kappa B DNA binding, inducing profuse levels of apoptosis and inhibiting mutagenesis. Even though further unsolved issues are awaited before phytoceuticals are accepted as a standard treatment for H. pylori infection, phytoceuticals can be a mighty weapon for either suppressing or modulating the disease-associated footprints of H. pylori infection. [source] Rabeprazole treatment attenuated Helicobacter pylori -associated gastric mucosal lesion formation in Mongolian gerbilsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2003HIDEKAZU SUZUKI Abstract Background and Aim: Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacter pylori (H. pylori), no studies have been conducted regarding the effect of RPZ on gastric mucosal lesion formation caused by this bacterium. In the present study, we investigated the effect of RPZ on H. pylori -associated gastric mucosal lesion formation. Methods: Sixty-two male Mongolian gerbils were inoculated with H. pylori (ATCC43504) (Hp group) and 60 gerbils with the culture media alone (control group). Some gerbils in the Hp group and in the control group were injected with RPZ (1 mg/kg/day, for 7 days) at the 5th week. Gerbils were evaluated at the 12th, 24th and 48th weeks. Results: In the Hp group, all gerbils were persistently infected for 24 weeks, but 36% became negative for H. pylori at the 48th week. In the Hp + RPZ group, 18% of gerbils at the 12th week, 40% at the 24th week, and 80% at the 48th week, became negative for H. pylori. The level of neutrophil infiltration was significantly decreased in the Hp + RPZ group in comparison to the Hp group, possibly through the effects of RPZ on initial bacterial colonization and resultant inflammation. Even in the gerbils that became H. pylori -negative, the level of neutrophil infiltration was lower in the Hp + RPZ group than in the Hp group. RPZ treatment significantly increased the level of the reduced form of glutathione (GSH) at the 48th week. The elevated levels of the reduced form of GSH may have been reduced by an antioxidation process in the H. pylori -positive Hp + RPZ group. Conclusion: Administration of RPZ not only inhibited gastric H. pylori colonization, but also reduced gastric mucosal inflammation in gerbils, possibly through its antibacterial action as well as pharmacological recruitment of the reduced form of GSH. © 2003 Blackwell Publishing Asia Pty Ltd [source] Dynamics of Helicobacter pylori infection in early childhood in a high-risk group living in Germany: loss of infection higher than acquisitionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2002D. Rothenbacher SUMMARY Background : The dynamics of Helicobacter pylori infection in early childhood are not yet well understood. Aim : To conduct a prospective study in a population of children known to be at high risk of H. pylori infection to elucidate the incidence and loss of infection in childhood. Methods : Asymptomatic Turkish children [aged 1 (n = 56 children), 2 (n = 55 children) and 4 years (n = 69 children)] at baseline, on whom participating paediatricians had performed routine health screening examinations between September 1997 and October 1998, were included in the study. A follow-up was performed about 1 year later. The infection status was defined by means of an antigen-based stool assay. Results : In total, for 137 of 180 (76%) children, follow-up information was available. At baseline examination, the prevalence of infection in children with follow-up information was 27%[95% confidence interval (CI), 20,35%]. The incidence of H. pylori infection amongpreviously uninfected children was 7% (95% CI, 3,14%) and the loss of infection among previously infected children was 35% (95% CI, 20,54%) during follow-up. Conclusions : This prospective cohort study in a high-risk group of children living in Germany showed that H. pylori colonization may often not persist at an early age. Furthermore, the use of penicillins and macrolides may be associated with the loss of infection at an early age. [source] Influence of risk factors on endoscopic and clinical ulcers in patients taking rofecoxib or ibuprofen in two randomized controlled trialsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2001C. J. Hawkey Background: Highly selective inhibitors of the inducible cyclooxygenase-2 enzyme (coxibs) have been associated with less gastrotoxicity than nonselective NSAIDs in clinical studies. Aim: To evaluate the influence of risk factors for NSAID-induced gastrotoxicity on endoscopic and clinical ulcers in patients taking rofecoxib or ibuprofen. Methods: We analysed pooled data from two identical double-blind, randomized, 12-week endoscopy studies which compared the gastroduodenal toxicity of placebo (n=371), rofecoxib 25 mg (n=390), rofecoxib 50 mg (n=379), and ibuprofen 2400 mg daily (n=376) in patients with osteoarthritis. The potential risk factors evaluated were: age (< 65, , 65 years), sex, race (white, nonwhite), Helicobacter pylori status, presence of gastroduodenal erosions at baseline, a history of upper gastrointestinal disease, prior NSAID use within 30 days of study entry, and smoking. We also evaluated these factors for possible association with the development of clinically-evident gastrointestinal perforations, ulcers or bleeds over 12 weeks. Results: Across all treatment groups, the likelihood of detecting endoscopic ulcers, or of clinical presentation with a bleed, over 12 weeks was increased approximately 4,5-fold in patients with previous upper gastrointestinal disease (relative risk [95% confidence interval] of 4.2 [2.5, 7.1] for endoscopic ulcers; 3.8 [1.4, 10.6] for bleeds), or those with gastroduodenal erosions at baseline endoscopy (relative risk of 4.4 [2.6, 7.5] for endoscopic ulcers; 5.0 [1.9, 13.5] for bleeds). H. pylori infection did not increase the risk of endoscopic ulcers or bleeds (relative risk of 1.1 [0.8, 1.6] for endoscopic ulcers; 0.3 [0.1, 0.9] for bleeds). The risk factor sub-group effects were constant across all treatment groups, and the significantly higher incidence of ulcers with ibuprofen as compared to rofecoxib and placebo was maintained in all risk factor subgroups. Conclusions: Gastroduodenal erosions at baseline and a clinical history of upper gastrointestinal disease, but not H. pylori colonization, increased the risk for endoscopically-detected ulcers and clinical bleeds. Rofecoxib did not magnify the risk in any of the patient subgroups studied. [source] Determination of Helicobacter pylori in patients with chronic nonspecific pharyngitisTHE LARYNGOSCOPE, Issue 8 2009Zeynep K, lkaya Kaptan MD Abstract Objectives/Hypothesis: To determine if there is a relationship between Helicobacter pylori colonization in the pharynx mucous membrane and chronic nonspecific pharyngitis. Study Design: A prospective clinical study. Methods: Seventy patients with chronic pharyngitis and 20 healthy control subjects were examined with polymerase chain reaction (PCR) and culture for H. pylori colonization in the pharynx mucous membrane between March 2008 and October 2008. Patients with pharyngitis were seperated into two groups (35 patients in each) by using C-14 urea breath test, according to the presence of gastric H. pylori infection. Results: In the control group, none of the patients had H. pylori in the pharynx. In the chronic pharyngitis group, in 12 patients (34.3%) with gastric H. pylori infection and in seven patients (20%) without gastric infection, H. pylori colonization in pharynx mucosa was determined with the PCR method. In only two of chronic pharyngitis patients (5.8%), H. pylori infection was detected with culture. In the pharynx mucosa, the H. pylori infection rate was significantly higher in the chronic pharyngitis groups than in the control group (P = .002 between C-14 positive and control groups, P = .040 between C-14 negative and control groups). There was not a significant difference in H. pylori colonization in the pharynx of patients who had chronic pharyngitis with or without gastric ailments and H. pylori infection (P = .179). Conclusions: Chronic nonspecific pharyngitis without gastric H. pylori infection is significantly related to H. pylori colonization in the pharynx, and gastric involvement increases the rate of this spread. The gold standart for detection of H. pylori infection is the PCR method. Laryngoscope, 2009 [source] | ||||||||||