title: Reduced tissue immigration of monocytes by neuropeptide Y during endotoxemia is associated with Y2 receptor activation.
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 Y2 receptor-mediated effect on monocytes. Thus, NPY treatment has profound receptor-specific effects on the migration and adhesion of leukocytes under endotoxemic conditions.
authors.affiliation: Department of Functional and Applied Anatomy, Hannover Medical School, Carl-Neuberg-Str.1, 30625 Hannover, Germany. nave.heike@mh-hannover.de
authors.forename: Heike
authors.initials: H
authors.lastname: Nave
authors.forename: Sammy
authors.initials: S
authors.lastname: Bedoui
authors.forename: Frank
authors.initials: F
authors.lastname: Moenter
authors.forename: Jan
authors.initials: J
authors.lastname: Steffens
authors.forename: Melanie
authors.initials: M
authors.lastname: Felies
authors.forename: Thomas
authors.initials: T
authors.lastname: Gebhardt
authors.forename: Rainer H
authors.initials: RH
authors.lastname: Straub
authors.forename: Reinhard
authors.initials: R
authors.lastname: Pabst
authors.forename: Mira
authors.initials: M
authors.lastname: Dimitrijevic
authors.forename: Stanislava
authors.initials: S
authors.lastname: Stanojevic
authors.forename: Stephan
authors.initials: S
authors.lastname: von Hörsten
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D002448:Cell Adhesion / Q000187:drug effects / Q000235:genetics; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte / Q000187:drug effects* / Q000276:immunology; D015536:Down-Regulation / Q000187:drug effects / Q000276:immunology; D019446:Endotoxemia / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D005434:Flow Cytometry; D005609:Free Radicals / Q000378:metabolism; D007275:Injections, Intravenous; D007970:Leukopenia / Q000139:chemically induced / Q000503:physiopathology; D008070:Lipopolysaccharides; D008297:Male; D009000:Monocytes / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D009478:Neuropeptide Y / Q000378:metabolism / Q000494:pharmacology*; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D017476:Receptors, Neuropeptide Y / Q000235:genetics / Q000378:metabolism*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism
chemical_list: D005609:Free Radicals; D008070:Lipopolysaccharides; D009478:Neuropeptide Y; D012333:RNA, Messenger; D017476:Receptors, Neuropeptide Y; D014409:Tumor Necrosis Factor-alpha; C095889:neuropeptide Y2 receptor