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Neutrophil Activity (neutrophil + activity)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

ADAM17 activity during human neutrophil activation and apoptosis

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2006
Bruce Walcheck Dr.
Abstract Substrates of the metalloprotease ADAM17 (also known as TNF-, converting enzyme or TACE) undergo ectodomain shedding and include various inflammatory modulators. Though polymorphonuclear leukocytes contribute significantly to inflammation, direct analyses of ADAM17 on human neutrophils are very limited. In addition, the current understanding of the processes regulating ADAM17 activity primarily relate to its rapid activation. Therefore, to extend insights into the mechanisms of ADAM17 activity, we examined its surface expression and the shedding of its substrates during extended periods of neutrophil activation and apoptosis. Contrary to studies with immortalized hematopoietic cell lines, we report that surface expression of ADAM17 is maintained by human neutrophils activated with formyl peptides or by FcR/complement receptor-mediated phagocytosis. Interestingly, bacterial phagocytosis resulted in a significant increase in ADAM17 expression several hours after pathogen engulfment. We provide novel evidence that ADAM17 surface expression is also maintained during spontaneous and anti-Fas-induced neutrophil apoptosis. The well-validated ADAM17 substrates L-selectin and proTNF-, were shed efficiently by neutrophils under each of the conditions tested. Our data thus indicate prolonged ADAM17 expression during neutrophil effector functions. The implications of this may be a role by ADAM17 in both the induction and down-regulation of neutrophil activity. [source]

Impact of Helicobacter pylori on the Development of Vitamin B12 Deficiency in the Absence of Gastric Atrophy

HELICOBACTER, Issue 6 2002
Ender Serin
Abstract Background. Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. Materials and Methods. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori -infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. Results. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p < .01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p < .001). Conclusion. The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with nonulcer dyspepsia and minimal or no gastric atrophy. [source]

cag Pathogenicity Island of Helicobacter pylori in Korean Children

HELICOBACTER, Issue 4 2002
Jae Sung Ko
Abstract Background.cag pathogenicity island is reported to be a major virulence factor of Helicobacter pylori. The aim of this study was to investigate the status of cag pathogenicity island genes and gastric histology in Korean children with H. pylori gastritis. Methods.Helicobacter pylori DNA was extracted from antral biopsy specimens from 25 children with H. pylori gastritis. Specific polymerase chain reaction assays were used for four genes of cag pathogenicity island. The features of gastritis were scored in accordance with the updated Sydney System. Results.cagA was present in 23 (92%) of 25 children, and cagE in 24 (96%). Twenty-two (88%) children were cagT positive and 19 (76%) virD4 positive. All of the selected genes of the cag pathogenicity island were present in 17 (68%) children and completely deleted in one child. There were no differences in neutrophil activity and chronic inflammation between children infected with intact cag pathogenicity island strains and those with partially or totally deleted- cag pathogenicity island strains. Conclusion.cag pathogenicity island is not a uniform, conserved entity in Korea. Completeness of cag pathogenicity island may not be the major factor to determine the severity of H. pylori gastritis in children. [source]

Inhibition of the initial wave of NF-,B activity in rat muscle reduces ischemia/reperfusion injury

MUSCLE AND NERVE, Issue 4 2001
Sean T. Lille MD
Abstract Nuclear factor kappaB (NF-,B) is thought to play an important role in the expression of genes expressed in response to ischemia/reperfusion (I/R) injury. In this report, the activation of NF-,B in rat skeletal muscle during reperfusion following a 4-h ischemic period was studied. NF-,B activation displayed a biphasic pattern, showing peak activities from 30 min to 3 h postperfusion and 6 h to 16 h postperfusion, with a decline to baseline binding activity levels between 3 h and 6 h. Inhibition of NF-,B activation was investigated using proline dithiocarbamate (Pro-DTC). NF-,B binding activity during reperfusion was significantly reduced by intravenous administration of Pro-DTC. Additionally, Pro-DTC resulted in decreased muscle edema and neutrophil activity, with an increased percentage of muscle survival compared with vehicle controls. These results demonstrate that NF-,B is activated during reperfusion in a biphasic manner and that the regulation of the initial phase of NF-,B activation affords physiological protection against a severe ischemic stress. Selective inhibition of NF-,B during early reperfusion may therefore be a therapeutic intervention for I/R injury. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 534,541, 2001 [source]