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  • Phorbol ester  (1)
  • Substance P  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Stimulation and release of interleukin-1 from peritoneal macrophages of the mouse (1994)
    Springer
    Inflammation research 42 (1994), S. 154-158 
    Details
    ISSN: 1420-908X
    Keywords: Interleukin-1 ; Mouse macrophages ; Tumour necrosis factor ; Calcium ionophores ; Lipopoly-saccharide ; Phorbol ester
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lipopolysaccharide (LPS) caused a concentration-dependent increase of released and cell-associated interleukin-1 (IL-1) in resident peritoneal macrophages from the mouse. LPS was about 30 times more potent at stimulating the level of cell-associated IL-1 than it was at stimulating the release of IL-1. Human recombinant tumour necrosis factor-α (TNF-α) and the calcium ionophores A23187 and ionomycin induced a concentration-dependent increase of cell-associated IL-1 but failed to cause release of IL-1 at concentrations producing maximal stimulation of cell-associated IL-1. The phorbol ester, 4β-phorbol dibutyrate, stimulated the release of IL-1 from mouse macrophages but failed to induce an increase in cell-associated IL-1. Substance P, neurokinin A, neurokinin B, calcitonin gene-related peptide and platelet-activating factor did not increase the released or cell-associated IL-1 in mouse macrophages. These agents also failed to alter released or cell-associated IL-1 stimulated by LPS, 1 μg ml−1. It appears that a calcium signal is sufficient for the transcription and translation of IL-1 mRNA but does not result in the secretion of biologically active forms of IL-1. Our data also indicate that different intracellular signals may control the release and the cell accumulation of IL-1. We conclude that inflammatory mediators may independently increase either the release of, or the cell accumulation of IL-1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01983483
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    On the actions of substance P, somatostatin, and vasoactive intestinal polypeptide on rat peritoneal mast cells and in human skin (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 364-368 
    Details
    ISSN: 1432-1912
    Keywords: Substance P ; Somatostatin ; Vasoactive intestinal polypeptide ; Human skin ; Mast cells ; Compound 48/80
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1) Substance P (SP), somatostatin (Som), and vasoactive intestinal polypeptide (VIP) induced a concentration-dependent release of histamine from isolated rat peritoneal mast cells. 2) The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [d-Pro4,d-Trp7,9,10]-SP4–11 (SP-A) (10 μM), and also by benzalkonium chloride (10 μM). In addition, SP-A inhibited histamine release induced by compound 48/80, whilst that induced by goat anti-(rat-IgE) was unaffected. 3) In human skin, intradermal injection of SP, Som, or VIP produced flare and wheal responses. The flares to all three peptides were inhibited by preinjection of the skin with SP-A (25 pmol), whilst the wheal responses were unaffected. 4) It is concluded that the receptors mediating histamine release and the flare response are similar, and that SP, Som, and VIP are acting at a similar receptor to produce these effects. It is probable that this receptor is also the site of action of compound 48/80.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500821
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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