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Reduced tissue immigration of monocytes by neuropeptide Y during endotoxemia is associated with Y-2 receptor activation
dc.creator | Nave, H. | |
dc.creator | Bedoui, Sammy | |
dc.creator | Moenter, F. | |
dc.creator | Steffens, J. | |
dc.creator | Felies, M. | |
dc.creator | Gebhardt, Thomas | |
dc.creator | Straub, RH | |
dc.creator | Pabst, R. | |
dc.creator | Dimitrijević, Mirjana | |
dc.creator | Stanojević, Stanislava | |
dc.creator | von Hoersten, Stephan | |
dc.date.accessioned | 2021-02-18T10:26:39Z | |
dc.date.available | 2021-02-18T10:26:39Z | |
dc.date.issued | 2004 | |
dc.identifier.issn | 0165-5728 | |
dc.identifier.uri | http://intor.torlakinstitut.com/handle/123456789/175 | |
dc.description.abstract | Neuropeptide Y (NPY) increases survival in experimental septic shock, which might be mediated by cardiovascular and/or immunological effects. To study the latter hypothesis, we monitored blood leukocyte subsets over 96 h after intravenous (i.v.) application of LPS in chronically i.v.-cannulated rats. LPS induced a dramatic leukopenia at 4 h after challenge, which was blunted in NPY-treated animals by stabilizing granulocyte and T-lymphocyte numbers. In addition, NPY treatment prevented tissue immigration of monocytes at early time points and consecutively mobilized activated monocytes from the third day after challenge. RT-PCR and in vitro adhesion studies provided evidence for a NPY Y-2 receptor-mediated effect on monocytes. Thus, NPY treatment has profound receptor-specific effects on the migration and adhesion of leukocytes under endotoxemic conditions. (C) 2004 Elsevier B.V. All rights reserved. | en |
dc.publisher | Elsevier, Amsterdam | |
dc.rights | restrictedAccess | |
dc.source | Journal of Neuroimmunology | |
dc.subject | monocytes/macrophages | en |
dc.subject | rodent | en |
dc.subject | endotoxic shock | en |
dc.subject | cell trafficking | en |
dc.subject | lung | en |
dc.title | Reduced tissue immigration of monocytes by neuropeptide Y during endotoxemia is associated with Y-2 receptor activation | en |
dc.type | article | |
dc.rights.license | ARR | |
dc.citation.epage | 12 | |
dc.citation.issue | 1-2 | |
dc.citation.other | 155(1-2): 1-12 | |
dc.citation.rank | M22 | |
dc.citation.spage | 1 | |
dc.citation.volume | 155 | |
dc.identifier.doi | 10.1016/j.jneuroim.2004.05.009 | |
dc.identifier.pmid | 15342191 | |
dc.identifier.scopus | 2-s2.0-4444240980 | |
dc.identifier.wos | 000224003900001 | |
dc.type.version | publishedVersion |