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H. Pylori Bacteria (h + pylori_bacteria)
Selected AbstractsFlow cytometric analysis of the localization of Helicobacter pylori antigens during different growth phasesFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2001Kristina Blom Abstract Previous studies on the localization of several different Helicobacter pylori antigens have been contradictory. We have therefore examined by using both one- and two-color flow cytometry (FCM), immunofluorescence (IF), and immunoelectron microscopy (IEM), the possible surface localization of some H. pylori antigens that may be important virulence factors. All four methods detected the lipopolysaccharide and the N -acetyl-neuroaminyllactose-binding hemagglutinin protein (HpaA) as surface-exposed, while the urease enzyme was not detected at all and the neutrophil activating protein only in low concentration on the surface of the H. pylori bacteria during culture of H. pylori in liquid broth for 11 days. The FCM analysis was found to be quite sensitive and specific and also extremely fast compared with IF and IEM, and therefore the preferred method for detection of surface-localized antigens of H. pylori. [source] Interleukin-6 Induction by Helicobacter pylori in Human Macrophages is Dependent on PhagocytosisHELICOBACTER, Issue 3 2006Stefan Odenbreit Abstract Background:, The colonization of the gastric mucosa with Helicobacter pylori is accompanied by elevated levels of proinflammatory cytokines, such as interleukin-1 (IL-1), IL-6, and IL-8. The aim of our study was to determine the mechanisms of IL-6 stimulation in phagocytes upon H. pylori infection. Materials and Methods:, We investigated the secretion of IL-6 by different professional phagocytes from murine and human origin, including granulocyte- and monocyte-like cells and macrophages derived from human peripheral blood monocytes (PBMCs). The influence of viability, phagocytosis, and the impact of different subcellular fractions of H. pylori bacteria were evaluated. Results:, IL-6 levels induced by H. pylori were low in cell lines derived from murine and human monocytes and in human granulocyte-like cells. By contrast, macrophages derived from human PBMCs were highly responsive to both H. pylori and Escherichia coli. IL-6 induction was blocked by inhibition of actin-dependent processes prior to infection with H. pylori, but not with E. coli or E. coli lipopolysaccharide (LPS). Using cell fractionation, the most activity was found in the H. pylori membrane. H. pylori LPS exhibited a 103 - to 104 -fold lower biologic activity than E. coli LPS, suggesting a minor role for toll-like receptor 4 (TLR4)-mediated signalling from the exterior. Conclusions:, From these data, we conclude that macrophages may be a major source of IL-6 in the gastric mucosa upon H. pylori infection. The IL-6 induction by H. pylori in these cells is a multifactorial process, which requires the uptake and presumably degradation of H. pylori bacteria. [source] Mast cells and IgE-containing cells in gastric mucosa of Helicobacter pylori infected and non-infected patients with chronic urticariaJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 1 2004M Liutu ABSTRACT Background, Several studies have indicated that antibiotic therapy aimed at eradication of Helicobacter pylori has effects on symptoms of chronic urticaria (CU) patients. However, the possible connections and pathomechanism by which H. pylori might be linked to CU have remained largely unknown. The IgE-mediated pathway might be a possible link between H. pylori infection and CU. We therefore clarified the role of H. pylori as an inducer of IgE response. Materials and methods, Gastroscopy was performed and mucosal biopsy specimens were taken to evaluate the histology, as well as the presence of H. pylori bacteria, mast cells and IgE-containing cells in the antral mucosa, in 21 CU patients. Controls (n = 48) included 19 patients with lichen planus, nine patients with atopic dermatitis and 20 patients with no skin or allergic disease. Results, The mean densities of IgE-containing cells were significantly higher in H. pylori- infected patients and in patients with skin disease compared to non- H. pylori -infected patients with no skin or allergic disease. No significant difference was found in the number of IgE-containing cells between H. pylori -infected and non-infected patients with CU. There was no significant difference in the mean densities of mast cells in the different patient groups. Conclusions, Our findings suggest that H. pylori gastritis leads to increased IgE production. However, we could not show a significant difference in IgE staining between H. pylori -infected and non-infected patients with CU. [source] Double gastric infection with Helicobacter pylori and non- Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2001S. Sanduleanu Background: Long-term acid suppression may accelerate the development of atrophic gastritis in Helicobacter pylori -positive subjects. The pathogenetic mechanism remains unclear. Aim: To test the hypothesis that gastric double infection with H. pylori and non -H. pylori bacterial species,during acid suppression,may result in an enhanced inflammatory response, contributing to the development of atrophic gastritis. Patients and methods: A consecutive series of patients with gastro-oesophageal reflux disease undergoing treatment with proton pump inhibitors (n=113) or histamine2 -receptor antagonists (H2 -RAs) (n=37), and 76 non-treated dyspeptic controls were investigated. Gastric mucosal H. pylori and non- H. pylori bacteria, histological gastritis, H. pylori serology, and circulating interleukin (IL)-1,, IL-6, and IL-8 were examined. Results: Patients on acid suppression with either proton pump inhibitors or H2 -RAs had a similar prevalence of H. pylori infection to the controls, but a higher prevalence of non- H. pylori bacteria (61% and 60% vs. 29%, P < 0.0001 and P < 0.002). Both the presence of H. pylori and non- H. pylori bacteria were independent risk factors of atrophic gastritis (antrum: relative risks (RRs), 10.1 and 5.07; corpus: RRs, 11.74 and 6.38). A simultaneous presence of H. pylori and non- H. pylori bacteria was associated with a markedly increased risk of atrophic gastritis (antrum: RR, 20.25; corpus: RR, 20.38), compatible with a synergistic effect. Furthermore, the simultaneous presence of both types of bacteria was associated with higher cytokine levels than in patients without any type of bacteria. This increase was also greater than in patients with H. pylori infection alone (P < 0.001, for both IL-1, and IL-8). Summary and conclusions: H. pylori -positive patients on long-term acid inhibition displayed three features: non- H. pylori bacterial growth; increased cytokine levels; and a higher risk of atrophic gastritis. We suggest that double infection with H. pylori and non- H. pyloribacteria is a major factor in the development of atrophic gastritis during gastric acid inhibition. [source] | ||||||||||