Helicobacter pylori lipopolysaccharide provokes iNOS-mediated acute systemic microvascular inflammatory responses in rat cardiac, hepatic, renal and pulmonary tissues

Whittle, Brendan J.R.; Morschl, Éva; Pozsár, J; Moran, Anthony P.; László, Ferenc

doi:10.1016/s0928-4257(01)00035-3

Cited by 22 publications

(16 citation statements)

References 13 publications

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“…In inflamed tissue, NO is produced primarily by inducible NO synthase (iNOS) [106][107][108]. NO can also influence the microcirculation and may thereby also influence virus control [52,111,118,119].…”

Section: Nonimmunologic Molecules That Influence Virus Controlmentioning

confidence: 99%

Genes Determining the Course of Virus Persistence in the Liver: Lessons from Murine Infection with Lymphocytic Choriomeningitis Virus

Lang

Recher²,

Häussinger³

et al. 2010

Cell Physiol Biochem

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More than 500 million people worldwide are persistently infected with either hepatitis B virus (HBV) or hepatitis C virus (HCV). Although both viruses are poorly cytopathic, persistent infection causes severe immunopathologic damage to liver tissue; histologically, such damage is characterized by fatty liver disease, liver fibrosis, and a higher likelihood of hepatocellular carcinoma. Virus-specific CD8⁺ T cells play a crucial role during infection with hepatitis viruses. On the one hand, rapid activation of CD8⁺ T cells can control the virus and therefore inhibit its persistence. On the other hand, once the virus persists in the liver, the chronic activation of virus-specific T cells leads to continued liver cell damage. This double-edged role of CD8⁺ T cells determines the final outcome of infection. In half of cases of human HCV infection, the virus persists; in the other half, the virus is controlled. Additional insights into the molecular mechanisms that determine the course of the disease may be gained from the study of appropriate murine models. This review discusses the similarities and differences between infection with lymphocytic choriomeningitis virus (LCMV) in mice and chronic infection with hepatitis virus in humans.

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Section: Nonimmunologic Molecules That Influence Virus Controlmentioning

confidence: 99%

Genes Determining the Course of Virus Persistence in the Liver: Lessons from Murine Infection with Lymphocytic Choriomeningitis Virus

Lang

Recher²,

Häussinger³

et al. 2010

Cell Physiol Biochem

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“…It has been shown that H. pylori LPS is one of the virulence factors involved in the induction of gastritis. H. pylori LPS-dependent activation of monocytes and gastric epithelial cells leads to the production of several proinflammatory cytokines (11)(12)(13), oxygen radicals (14,15), and inducible NO (16). However, little detail is known about the recognition system for H. pylori LPS and its related intracellular signaling in gastric mucosal cells.…”

Section: Essential Role Of Md-2 In Tlr4-dependent Signaling Duringmentioning

confidence: 99%

Essential Role of MD-2 in TLR4-Dependent Signaling during Helicobacter pylori-Associated Gastritis

Ishihara

Rumi

Kadowaki

et al. 2004

The Journal of Immunology

146

138

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TLR4, a member of pattern recognition receptors, is the main receptor of LPS. MD-2 physically associates with TLR4 on the cell surface and confers LPS responsiveness. Helicobacter pylori LPS is one of the major virulence factors for induction of gastritis. We demonstrated in this study the role of MD-2 in TLR4-dependent signaling in H. pylori-associated gastritis. Gastric biopsy samples collected from patients with and without H. pylori infection and four gastric cancer cell lines were used for this study. TLR-4 and MD-2 expression in biopsy specimens and the cell lines was examined by using RT-PCR. Localization of TLR-4 in histological sections was evaluated by immunohistochemistry. For in vitro functional assays, we established stable transfectants of AGS cells expressing TLR4 and MD-2. Cellular distribution of TLR4 was examined by flow cytometry. NF-κB activation and activation of IL-8 and MD-2 promoters were assessed by reporter gene assay. H. pylori infection up-regulated the TLR4 and MD-2 expression in gastric mucosa. TLR4 staining was observed predominantly in epithelial cells, located in both the cytoplasm and at the apical surface. MD-2 transfection in AGS cells markedly increased cell surface expression of TLR4 and augmented the activation of NF-κB and IL-8 promoter upon stimulation with H. pylori LPS. Live H. pylori also stimulated transcriptional activation of MD-2. This study revealed that MD-2 expression is elevated in gastric epithelial cells during H. pylori infection, suggesting that the TLR4/MD-2 system is a potent receptor complex involved in the response to H. pylori LPS in the stomach.

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“…The method involved the conversion of L-["%C]arginine into L-["%C]citrulline using modifications [20,21] of the method described by Salter et al [22]. NOS activity was expressed in units of pmol : h −" : mg −" protein.…”

Section: Measurement Of Nos Activitymentioning

confidence: 99%

Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide

Babai¹,

SZIGETI²,

Parratt³

et al. 2002

Clinical Science

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Dogs were subjected to exercise on a treadmill, using a protocol in which the speed and slope were increased every 3 min, and which elevated both heart rate (to a mean of 198+/-14 beats.min(-1)) and mean arterial blood pressure (to 150+/-4 mmHg). Then, 24 or 48 h later, the dogs were anaesthetized with a mixture of alpha-chloralose and urethane and subjected to a 25 min occlusion of the left anterior descending coronary artery. The control dogs (instrumented but not exercised) were subjected to the same procedure. In some dogs the nitric oxide synthase inhibitor aminoguanidine (50 mg.kg(-1); intravenous) was administered 30 min before occlusion. Baroreflex sensitivity (BRS) was determined by the rapid bolus injection of phenylephrine 60 min before, and again 3 min after, the onset of occlusion. Exercise markedly reduced the consequences of coronary artery occlusion 24 h (but not 48 h) later, without modifying myocardial tissue blood flow. In the exercised dogs there were reductions in arrhythmia severity [ventricular fibrillation (VF) during occlusion, 0%; survival from the combined ischaemia/reperfusion insult, 70%] compared with controls (VF during occlusion, 36%; survival, 9%). BRS was preserved during occlusion in the exercised dogs (before occlusion, 1.60+/-0.54 ms.mmHg(-1); 3 min after occlusion, 1.37+/-0.4 ms.mmHg(-1)), but not in controls (before occlusion, 1.28+/-0.29 ms.mmHg(-1); 3 min after occlusion, 0.45+/-0.12 ms.mmHg(-1); P<0.05), and other ischaemic changes (inhomogeneity of electrical activation and changes in the ST-segment, recorded over the ischaemic region) were also less marked in the exercised dogs. Exercise-induced cardioprotection was abolished by aminoguanidine (VF during occlusion, 25%; survival, 0%). The results show that even a single period of exercise affords delayed protection against ischaemia/reperfusion-induced VF and other ischaemic changes. Since this protection is abolished by aminoguanidine, and since (inducible) NO synthase activity was elevated 3-fold in left ventricular samples 24 h after exercise, we suggest that this protection is mediated by nitric oxide.

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Helicobacter pylori lipopolysaccharide provokes iNOS-mediated acute systemic microvascular inflammatory responses in rat cardiac, hepatic, renal and pulmonary tissues

Cited by 22 publications

References 13 publications

Genes Determining the Course of Virus Persistence in the Liver: Lessons from Murine Infection with Lymphocytic Choriomeningitis Virus

Genes Determining the Course of Virus Persistence in the Liver: Lessons from Murine Infection with Lymphocytic Choriomeningitis Virus

Essential Role of MD-2 in TLR4-Dependent Signaling during Helicobacter pylori-Associated Gastritis

Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide

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