Expression of adhesion molecules on human granulocytes after stimulation with Helicobacter pylori membrane proteins: comparison with membrane proteins from other bacteria

Enders, G.; Brooks, William P.; Jan, N von; Lehn, Norbert; Bayerdörffer, Ekkehard; Hatz, R.

doi:10.1128/iai.63.7.2473-2477.1995

Cited by 44 publications

(30 citation statements)

References 33 publications

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“…Thus, it is not surprising that we found CD11c on neutrophils induced by H. pylori sonicate as well. In an assay closely related to ours, Enders et al [11] were not able to induce CD11c up-regulation by H. pylori extracts, but minor differences in concentrations, strains or experimental conditions could explain the lack of agreement. The change in CD11b expression was higher than that of CD11c, which may reflect the relative importance of the two membrane structures to the migration of the neutrophils across the endothelium [10].…”

Section: Discussionsupporting

confidence: 47%

“…By use of in vivo blocking MoAbs towards neutrophil adherence molecules, a reduced adherence of neutrophils to endothelium was demonstrated for both CD11b and CD11a (LFA-1) with no up-regulation for the latter marker [10]. No changes in the number of CD62L expressed on the cellular membrane could be demonstrated for neutrophils stimulated with H. pylori sonicate [11].…”

Section: Introductionmentioning

confidence: 95%

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Inflammatory activation of neutrophils by Helicobacter pylori; a mechanism insensitive to pertussis toxin

Hansen

Madsen

Petersen

et al. 2001

Clinical and Experimental Immunology

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SUMMARYChronic active gastritis of the antral mucosa is a characteristic feature of infection with Helicobacter pylori and interactions between bacterial components and inflammatory cells are believed to play an important pathogenic role. Neutrophils stimulated with H. pylori sonicate were demonstrated to release l-selectin (CD62L) expressed on the cellular surface, with a subsequent up-regulation of the b 2 -integrins CD11b and CD11c, both in a dose-and time-dependent manner, reaching maximum levels after 45±60 min of stimulation. No changes were observed for the CD11a receptor upon stimulation. The activating properties of H. pylori sonicates on neutrophils were heat-labile and susceptible to protease attack, indicating the protein nature of the activating factor. After size fractionation, the major neutrophil-inducing activity was detected in the high molecular weight fraction exhibiting urease activity. Pertussis toxin was unable to inhibit neutrophil activation by the H. pylori protein(s). We conclude that proteins from H. pylori have a potent inflammatory effect on the surface membrane molecules CD62L, CD11b and CD11c essential for transendothelial migration of neutrophils to areas of inflammation. The neutrophil-activating protein(s) act via a pertussis toxin-insensitive mechanism.

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Section: Discussionsupporting

confidence: 47%

Section: Introductionmentioning

confidence: 95%

Inflammatory activation of neutrophils by Helicobacter pylori; a mechanism insensitive to pertussis toxin

Hansen

Madsen

Petersen

et al. 2001

Clinical and Experimental Immunology

View full text Add to dashboard Cite

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“…Helicobacter pylori is the most important cause of chronic active gastritis and gastric and duodenal ulcers, and plays an important role in the development of gastric cancer and mucosa associated lymphoid tissue (MALT) lymphomas (Graham et al, 1991;Parsonnet et al, 1991;Kreiss et al, 1995). The acute H. pylori infection induces mucosal infiltration dominated by neutrophil leucocytes initiated by invasive H. pylori or water-soluble proteins passing the mucosal barrier (Bode et al, 1987;Andersen & Holck, 1990;Enders et al, 1995). Within a few weeks, the acute inflammation develops to chronic active inflammation dominated by neutrophils, macrophages (CD14), lymphocytes (CD4, CD8 and CD19) and plasma cells (Bode et al, 1987;Andersen & Holck, 1990;Dixon et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Gastric inflammatory markers and interleukins in patients with functional dyspepsia treated with astaxanthin

Andersen

Holck

Kupčinskas³

et al. 2007

FEMS Immunol Med Microbiol

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The chronic active inflammation caused by Helicobacter pylori is dominated by neutrophils, macrophages, lymphocytes and plasma cells. Several interleukins are involved in the inflammatory process. The aim of this study was to investigate the effect of astaxanthin on gastric inflammation in patients with functional dyspepsia. Forty-four consecutive patients were included, and biopsies were examined for IL-4, IL-6, IL-8, IL-10, interferon-gamma, CD4, CD8, CD14, CD19, CD25 and CD30. Patients were randomized: 21 patients were treated with 40 mg of astaxanthin daily, and 23 patients were treated with a placebo. There was a significant decrease in gastric inflammation in H. pylori-positive patients from both groups. There were no significant changes in the density of H. pylori or in any of the interleukins during or after treatment. There was a significant up-regulation of CD4 and down-regulation of CD8 in patients with H. pylori treated with astaxanthin. Astaxanthin had an effect on the inflammation and on the density of H. pylori in mice in a study where the diet could be standardized without antioxidants (Bennedsen et al., 1999). These dietary conditions are impossible in studies involving humans, and may be due to the minor effect when the host have access to antioxidants in their diet.

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“…The acute H. pylori infection induces mucosal infiltration dominated by neutrophil leucocytes. Within few weeks, the acute inflammation develops to chronic active inflammation dominated by neutrophils, macrophages (CD14), lymphocytes (CD4, CD8 and CD19) and plasma cells [4,5]. The initiation of the inflammation may be caused by invasive H. pylori or water‐soluble proteins passing the mucosal barrier [5–7].…”

Section: Introductionmentioning

confidence: 99%

Gastric inflammatory markers and interleukins in patients with functional dyspepsia, with and withoutHelicobacter pyloriinfection

Andersen

Holck

Janulaitytė-Gunther³

et al. 2005

FEMS Immunology &Amp; Medical Microbiology

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Helicobacter pylori is the most important cause of gastritis, peptic ulcers and the development of gastric cancer. The chronic active inflammation is dominated by neutrophils, macrophages, lymphocytes and plasma cells. Several interleukins (IL-8, IL-10 and IFN-gamma) are involved in the inflammatory process in the gastric mucosa. The aim of this study was to investigate the gastric inflammation in patients with functional dyspepsia. Fifty-three consecutive patients were included and antral biopsies were obtained for histology, culture and immunohistochemistry. The sections were examined for the interleukins IL-4, IL-6, IL-8, IL-10 and IFN-gamma as well as for the cell markers CD4, CD8, CD14, Cd19, CD25 and CD30. Only CD4 and CD19 were significantly increased in patients with increased gastric inflammation and increased density of H. pylori. However, several of the examined markers (IFN-gamma, IL-8, IL-10 and CD14) showed a non-significant trend to be increased in patients with extensive gastric inflammation and high density of H. pylori. Therefore, an arbitrary index (IM11) for all the 11 immunological markers was made as an average value for each of the four morphological groups. For the four morphologically different groups of patients the values were 0.49, 0.77, 0.86 and 1.25, respectively. Significant increases in the index from none to moderate antral inflammation as well as the density of H. pylori were found (p<0.001). By using an index of inflammatory markers trends can be summarized and thereby significant which may be of importance when gastric inflammation is investigated in children and patients with functional dyspepsia.

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Expression of adhesion molecules on human granulocytes after stimulation with Helicobacter pylori membrane proteins: comparison with membrane proteins from other bacteria

Cited by 44 publications

References 33 publications

Inflammatory activation of neutrophils by Helicobacter pylori; a mechanism insensitive to pertussis toxin

Inflammatory activation of neutrophils by Helicobacter pylori; a mechanism insensitive to pertussis toxin

Gastric inflammatory markers and interleukins in patients with functional dyspepsia treated with astaxanthin

Gastric inflammatory markers and interleukins in patients with functional dyspepsia, with and withoutHelicobacter pyloriinfection

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