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  • 1
    Electronic Resource
    Electronic Resource
    Helicobacter pylori Outer Membrane Protein 18 (Hp1125) Induces Dendritic Cell Maturation and Function (2005)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 10 (2005), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  Dendritic cells (DCs) are potent antigen-presenting cells that initiate T-cell responses. A robust adaptive Th1 immune response is crucial to an adaptive (Th2) immune response necessary for vaccine-induced protective immunity against Helicobacter pylori. It has been shown that several outer membrane proteins (Omps) induce a robust antibody response. However, it is also known that the antibodies generated are not protective. Moreover there is great variation in the recognition of high molecular weight H. pylori proteins by sera from infected patients. In contrast to the high molecular weight proteins, serologic responses to small molecular weight proteins provide assessment of current infection with H. pylori and also of its eradication.Aim.  The goal of the study was to analyze the activation of the immune response by a specific low molecular weight Omp that is universally expressed by all H. pylori strains. Therefore, we studied interaction of H. pylori Omp18 with DCs.Methods.  Activation of murine bone marrow-derived DCs and production of cytokines by Omp18 was assessed by fluorescence-activated cell sorter (FACS) for costimulatory markers and ELISA, respectively. The ability of Omp18 stimulated DCs to induce lymphocyte proliferation was measured in a mixed leukocyte reaction.Results.  Omp18 induced higher expression of the B7 (CD80 and CD86) costimulatory molecule after 18 hours indicating processing and presentation of the antigen on the surface by bone marrow-derived DCs. The maturing DCs also secreted significant levels of IL-12, but was 4-fold less than that stimulated by whole bacteria. Omp18-primed DCs induced proliferation and release of IFNγ by syngeneic splenocytes.Conclusion.  We concluded that Omp18 is capable of activating DCs initiating a Th1 immune response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1523-5378.2005.00350.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanism of intragastric tetramethylammonium protection against 40% ethanol injury in rat stomach (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 708-712 
    Details
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol-induced gastric mucosal injury ; tetramethylammonium ; gastric mucus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of tetramethylammonium (TMA), a ganglionic stimulant, on gastric mucosal injury induced by 40% ethanol was examined. In studies I–III, rats were treated with intragastric vehicle or TMA (1 or 10 mg/kg). In study I, 1 hr after the treatment, 40% ethanol was given intragastrically. The length of the linear corpus mucosal lesions was measured unbiasedly with a caliper after another hour. In study II, mean blood pressure was assessed before and after the treatment. In study III, 1 hr after the treatment, gastric mucus and juice volumes, and titratable acid were measured. In study IV, 40% ethanol (10 ml/kg) was administered intragastrically immediately after 0.2 or 1.4 ml of intragastric vehicle treatment. One hour later, gastric lesion score was assessed as in study I. Results show that (1) intragastric TMA dose-dependently protected against 40% ethanol-induced gastric injury; (2) neither dose of intragastric TMA increased mean blood pressure; (3) there was a dose-related increase in gastric mucus secretion for TMA 1 and 10 mg/kg, and a significant increase in gastric juice volume only for TMA 10 mg/kg; and (4) the rats treated with 1.4. ml of vehicle plus 40% ethanol had significantly less injury than those treated with 0.2 ml of vehicle plus 40% ethanol. We conclude that the protective effect of intragastric TMA can be explained by its dose-related effect in enhancing gastric mucus secretion for TMA 1 and 10 mg/kg and the significantly greater increase in gastric juice volume for TMA 10 mg/kg. Even though parenteral TMA is a recognized ganglionic stimulant, the protective effect of intragastric TMA is unlikely to be due to its ganglionic stimulatory property, as neither 1 nor 10 mg/kg intragastric TMA increases mean blood pressure. However, the possibility that intragastric TMA acts as a local stimulant of intramural ganglia cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01316804
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  • 3
    Electronic Resource
    Electronic Resource
    Involvement of α2-Adrenoceptors in mechanism of intragastric nicotine protection against ethanol injury in rat stomach (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 713-721 
    Details
    ISSN: 1573-2568
    Keywords: α-adrenoceptors ; prazosin ; yohimbine ; β-adrenoceptors ; metoprolol ; butoxamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate the role of α- and β-adrenoceptors in the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury, the following studies were performed. At 0.5-hr prior to the injury study, rats were pretreated with: subcutaneous control, prazosin (0.5 mg/kg) or yohimbine (5 mg/kg) to block α1- or α2-adrenoceptors; or intraperitoneal control, metoprolol (2 mg/kg) or butoxamine (4 mg/kg) to block β1- or β2-adrenoceptors, respectively. At 1-hr intervals, rats received intragastric vehicle or nicotine (4 mg/kg) and 40% ethanol (10 ml/kg). Total lengths of the linear gastric corpus mucosal lesions were measured by an unbiased observer using a caliper. In a separate study, 0.5-hr after subcutaneous control or yohimbine (5 mg/kg), rats were treated with intragastric vehicle or nicotine (4 mg/kg). One hour later, gastric mucus volume, gastric juice volume and pH, and titratable acid in the gastric juice were measured. In the rat stomach, the intragastric nicotine protection against 40% ethanol-induced mucosal injury was not blocked by selective α1-(prazosin), β1-(metoprolol), or β2-(butoxamine) adrenoceptor antagonists. The protection was significantly reduced although not completely abolished by selective α2-(yohimbine) adrenoceptor antagonist. Yohimbine also significantly reduced basal and nicotine-stimulated increase in gastric mucus volume. These data suggest that α2-adrenoceptors are involved in the protective effect of intragastric nicotine against 40% ethanol-induced gastric mucosal injury possibly by a mucus-dependent mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01316805
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition of endogenous nitric oxide reduces basal mesenteric vascular tone but does not alter intraduodenal hydrochloric acid-induced intestinal hyperemia in rats (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 1729-1737 
    Details
    ISSN: 1573-2568
    Keywords: blood flow ; duodenum ; duodenal villous damage ; intestine ; NG-nitro-l-arginine methyl ester ; superior mesenteric artery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There are conflicting reports on the role of endogenous nitric oxide (NO) in the regulation of basal intestinal blood flow. The effect of inhibition of NO on intraduodenal hydrochloric acid (HCl) induced intestinal hyperemia remains to be confirmed. We investigated the effect of inhibition of endogenous NO on basal intestinal blood flow, HCl-induced intestinal hyperemia, and duodenal villous injury. Superior mesenteric artery blood flow in rats was measured by pulsed Doppler flowmetry and duodenal villous injury evaluated by histology. Intravenous NG-nitro-l-arginine methyl ester (l-NAME), orl-arginine ord-arginine followed byl-NAME, was given to show inhibition, reversal of inhibition of endogenous NO synthase, and stereospecificity, respectively. An intraduodenal 2 ml/kg bolus or perfusion for 30 min of 0.1 N HCl was given 15 min afterl-NAME or vehicle. Mean arterial blood pressure was increased byl-NAME, which also significantly reduced intestinal blood flow under basal condition and after intraduodenal HCl. Basal mesenteric blood flow was not altered byl- ord-arginine. Thel-NAME-induced increase in blood pressure and decrease in basal blood flow was attenuated byl- but notd-arginine. The villous damage and the magnitude of the peak hyperemia was unchanged byl-NAME,l- ord-arginine. Inhibition of endogenous NO byl-NAME is suggested by the significant rise in blood pressure. The rise in blood pressure and reduction in blood flow are attenuated byl- but notd-arginine, indicating stereospecificity. Inhibition of endogenous NO reduces basal mesenteric vascular tone but does not alter intraduodenal HCl-induced intestinal hyperemia. The increase in blood flow after intraduodenal HCl predicts the absence of exacerbation of HCl-induced duodenal villous damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02212694
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  • 5
    Electronic Resource
    Electronic Resource
    Intragastric nicotine protection against 40% ethanol injury in rat stomach (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 1840-1846 
    Details
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol-induced gastric mucosal injury ; hexamethonium ; mecamylamine ; gastric mucus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intragastric nicotine (4 mg/kg) protects against 40% ethanol-induced gastric mucosal injury and raises mean blood pressure. We postulated that this protective effect was mediated by the ganglionic stimulatory property of nicotine and therefore could be abolished by ganglionic blockers. Rats were pretreated with intraperitoneal hexamethonium (10 mg/kg) or mecamylamine (2 mg/kg) to block peripheral or central autonomic ganglia, respectively. Intragastric vehicle or nicotine (4 mg/kg) was then administered. The total lengths of the linear gastric corpus mucosal lesions induced by intragastric 40% ethanol were measured by an unbiased observer using a caliper. The results showed that both intraperitoneal hexamethonium and mecamylamine pretreatments protected against 40% ethanol-induced gastric mucosal injury. Neither modified the protective effect of intragastric nicotine. The protective effect of hexamethonium and mecamylamine was associated with a significant increase in the volume of gastric mucus and gastric juice. The increase in the volume of gastric content (mucus and juice) was partially responsible for the protective effect of these ganglionic blockers. In a separate experiment, intraperitoneal nicotine (4 mg/kg) also protected against 40% ethanol-induced gastric mucosal injury and raised mean blood pressure. These data indicate that the protection against 40% ethanol-induced gastric mucosal injury is not unique to intragastric nicotine. Such protection can be induced by ganglionic blocking doses of hexamethonium and mecamylamine, or a ganglionic stimulatory dose of intraperitoneally administered nicotine. Whether ganglionic stimulation or blockade plays a role in the mechanism of intragastric nicotine protection, however, remains to be determined. Further studies of the regulation of gastric mucus production and gastric juice volume may shed light on the mechanism of protection afforded by intragastric nicotine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01308077
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