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  • 1
    Electronic Resource
    Electronic Resource
    Attraction of human monocytes by the neuropeptide secretoneurin
    Amsterdam : Elsevier
    FEBS Letters 334 (1993), S. 41-44 
    Details
    ISSN: 0014-5793
    Keywords: Chemotaxis ; Monocyte ; Neurogenic inflammation ; Secretogranin II ; Secretoneurin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(93)81676-Q
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Inhibition of superoxide anion release from circulating neutrophils by l-arginine in man (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 985-989 
    Details
    ISSN: 1432-1440
    Keywords: Nitric oxide ; Respiratory burst ; Ischemia ; Reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In animal studies of myocardial ischemia/reperfusion l-arginine reduces necrotic injury by preservation of endothelial function and attenuation of neutrophil accumulation in ischemic cardiac tissue. Because release of oxygen radical species by circulating neutrophils is important in endothelial function and ischemia-reperfusion injury, this study investigated the effect of intravenous administration of L-arginine on the in vitro release of superoxide anion of neutrophils in healthy young adults. Neutrophils were obtained at various time points before, during, and after infusion of l-arginine (17 mg kg−1 min−1 for 30 min) and analyzed for superoxide dismutase inhibitable reduction of ferricytochrome c. The spontaneously occurring respiratory burst of polymorphonuclear leukocytes at basal conditions was compared with that after triggering by 1 μmol/l formylpeptide or 50 ng/ml phorbolester. Infusion of l-arginine inhibited both basal (P 〈 0.01) and formylpeptide-triggered (P 〈 0.05) release of superoxide anion did, but not affect release stimulated by phorbol 12-myristate 13-acetate. Pretreatment of neutrophils with 1 mmol/l l-arginine in vitro also significantly reduced formylpeptide-triggered (1 μmol/l) superoxide anion release, suggesting that the affects observed after in vivo pretreatment may be due to direct action of l-arginine on neutrophils. These findings demonstrate the ability of L-arginine to reduce release of oxygen radical species by circulating neutrophils in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180028
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  • 3
    Electronic Resource
    Electronic Resource
    Superoxide anion release from neutrophils in growth hormone deficient adults before and after replacement therapy with recombinant human growth hormone (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 369-373 
    Details
    ISSN: 1432-1912
    Keywords: Growth hormone deficiency ; Neutrophils ; Monocytes ; Respiratory burst ; Chemotaxis ; Treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The observations that growth hormone primes neutrophils and stimulates various activities of monocytes suggested that it plays a role in the regulation of leukocyte biology. The in vivo reduction of growth hormone levels may be responsible for to the functional impairment of leukocytes observed in growth hormone deficient children. Whether leukocyte function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophils and chemotaxis of monocytes in 15 patients with adult-onset growth hormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performed by comparing functions of the leukocytes from these patients with those from age and sex-matched healthy control subjects. Before growth hormone treatment, patients received appropriate replacement therapy with thyroid, adrenal and gonadal hormones. The dose of recombinant human growth hormone was 0.25–0.5 U/kg/week (0.013–0.026 mg/kg/day) throughout the whole period of replacement therapy. In growth hormone deficient subjects, formylpeptide-triggered release of superoxide anions from neutrophils was significantly suppressed by about 40% before treatment as compared to healthy control subjects. After 6 months of replacement therapy, neutrophil superoxide anion release was similar in patients and healthy individuals. Neither before nor after replacement therapy, however, was there a difference in monocyte migration between control and growth hormone deficient subjects. These data indicate that neutrophil function is somehow altered in growth hormone deficient patients, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to near normalcy by growth hormone replacement therapy. This would suggest that suppressed neutrophil respiratory burst is due to the deficiency in growth hormone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171070
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition of recombinant human growth hormone-induced and prolactin-induced activation of neutrophils by octreotide (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 336-341 
    Details
    ISSN: 1432-1912
    Keywords: Somatostatin ; Octreotide ; Neutrophils ; Raspiratory burst ; Chemotaxis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Growth hormone, prolactin and somatostatin are polypeptide hormones of the neuroendocrine and peripheral nervous systems. In vitro, these have opposing effects on cells of the immune system. We compared the effects of these peptides on activation of neutrophils using a recombinant preparation of human growth hormone, human prolactin and octreotide, a long acting analog of somatostatin. In the absence of growth hormone, octreotide did not affect either neutrophil locomotion or respiratory burst. Octreotide, however, significantly antagonized growth hormone-induced activation of neutrophils for enhanced respiratory burst as well as growth hormone-induced inhibition of stimulated migration. As the effect of growth hormone on neutrophils is mediated by the prolactin receptor, its inhibition by octreotide was also tested using prolactin as priming agent. Data indicate comparable effects of octreotide on priming of neutrophils by prolactin. The effect of octreotide was dose-dependent and appeared to be selective, as activation of neutrophil respiration burst by γ-interferon, and inhibition of stimulated migration by tumor necrosis factor-α were unaffected by octreotide. The present study suggests that octreotide may act on neutrophils directly by antagonizing growth hormone or prolactin at the cellular level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167454
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Superoxide anion release from neutrophils in growth hormone deficient adults before and after replacement therapy with recombinant human growth hormone (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 369-373 
    Details
    ISSN: 1432-1912
    Keywords: Key words Growth hormone deficiency ; Neutrophils ; Monocytes ; Respiratory burst ; Chemotaxis ; Treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The observations that growth hormone primes neutrophils and stimulates various activities of monocytes suggested that it plays a role in the regulation of leukocyte biology. The in vivo reduction of growth hormone levels may be responsible for to the functional impairment of leukocytes observed in growth hormone deficient children. Whether leukocyte function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophils and chemotaxis of monocytes in 15 patients with adult-onset growth hormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performed by comparing functions of the leukocytes from these patients with those from age and sex-matched healthy control subjects. Before growth hormone treatment, patients received appropriate replacement therapy with thyroid, adrenal and gonadal hormones. The dose of recombinant human growth hormone was 0.25–0.5 U/kg/week (0.013–0.026 mg/kg/day) throughout the whole period of replacement therapy. In growth hormone deficient subjects, formylpeptide-triggered release of superoxide anions from neutrophils was significantly suppressed by about 40% before treatment as compared to healthy control subjects. After 6 months of replacement therapy, neutrophil superoxide anion release was similar in patients and healthy individuals. Neither before nor after replacement therapy, however, was there a difference in monocyte migration between control and growth hormone deficient subjects. These data indicate that neutrophil function is somehow altered in growth hormone deficient patients, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to near normalcy by growth hormone replacement therapy. This would suggest that suppressed neutrophil respiratory burst is due to the deficiency in growth hormone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171070
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Effects of thalidomide on neutrophil respiratory burst, chemotaxis, and transmigration of cytokine- and endotoxin-activated endothelium (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 356 (1997), S. 529-535 
    Details
    ISSN: 1432-1912
    Keywords: Key words Neutrophils ; Endothelium ; Migration ; Thalidomide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vascular endothelium activated by endotoxin and cytokines plays an important role in organ inflammation and blood leukocyte recruitment. Neutrophils, which are a homogeneous population of effector cells, are rapidly attracted in large numbers to sites of inflammation where they form an early response to infection or injury. Excessive production of various interleukins, TNF, arachidonic acid metabolites, and other substances by neutrophils and macrophages results in systemic endothelial cell injury, a fundamental problem. In the present study, we investigated in vitro the effects of thalidomide (THD) on activation of endothelial cells for enhanced transmigration of neutrophils by lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF), and interleukin-1 (IL-1). Modulation of endotoxin- and cytokine-induced neutrophil chemotaxis and respiratory burst by THD were also studied. Treatment of HUVEC with THD in combination with LPS, TNF, and IL-1, respectively, antagonized LPS-activated transmigration of neutrophils but stimulated the effects of TNF and IL-1. All of the agents used – THD, LPS, TNF, and IL-1 – inhibited neutrophil chemotaxis. Addition of THD to the neutrophils had no effect on LPS-inhibited chemotaxis whereas the TNF- and IL-1-induced chemotaxis was modulated in a bimodal manner. However, THD failed to influence neutrophil respiratory burst activity. Results demonstrate that THD differentially affects mediator-induced activation of HUVEC and neutrophils.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005087
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