Cytokine and adhesion molecule requirements for neutrophil recruitment during glycogen-induced peritonitis
dc.contributor.author | Lentsch, Alex B. | en_US |
dc.contributor.author | Mulligan, Michael S. | en_US |
dc.contributor.author | Miyasaka, Masayuki | en_US |
dc.contributor.author | Ward, Peter A. | en_US |
dc.date.accessioned | 2006-09-08T19:40:17Z | |
dc.date.available | 2006-09-08T19:40:17Z | |
dc.date.issued | 1998-06 | en_US |
dc.identifier.citation | Mulligan, M. S.; Lentsch, A. B.; Miyasaka, M.; Ward, P. A.; (1998). "Cytokine and adhesion molecule requirements for neutrophil recruitment during glycogen-induced peritonitis." Inflammation Research 47(6): 251-255. <http://hdl.handle.net/2027.42/41819> | en_US |
dc.identifier.issn | 1023-3830 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/41819 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=9683032&dopt=citation | en_US |
dc.description.abstract | Objective: Requirements for cytokines and adhesion molecules for perititoneal neutrophil recruitment during glycogen-induced peritonitis in rats were systematically defined.¶ Subjects: Male Long Evans rats (275–300 g).¶ Methods: Four hours after intraperitoneal injection of 25 mg oyster glycogen, neutrophilic exudates were harvested. Effects of blocking reagents (injected intravenously) to rat E-, L- and P-selectins, β 1 (VLA-4) and β 2 integrins (LFA-1 and Mac-1), ICAM-1, and the cytokines TNFα, IL-1 and IL-8 were assessed.¶ Results: Administration of synthetic sialyl Lewis x oligosaccharide reduced neutrophil recruitment to the peritoneum by 26%. Antibody to E-selectin reduced neutrophil accumulation by 71%, while anti-L-selectin reduced neutrophil accumulation by 59%, and anti-P-selectin was without an effect. Similar patterns of inhibition were found when selectin-Ig chimeras were employed. Antibodies to LFA-1 (CD11a), Mac-1 (CD11b) or CD18 reduced neutrophil accumulation by 62%, 59% and 86%, respectively, while anti-VLA-4 was without effect. Anti-ICAM-1 reduced cell influx by 65%. IL-1 receptor antagonist and antibodies to IL-1 and human IL-8 reduced neutrophil accumulation by 43%, 40% and 62%, respectively. Unexpectedly, blockade of TNFα had no effect.¶ Conclusions: These studies identify requirements for selectins, β 2 integrins, IL-1 and a rat chemokine(s) similar to human IL-8 for neutrophil recruitment during glycogen-induced peritonitis. The lack of participation of VLA-4, P-selectin and TNFα suggests organ-specific cytokine and adhesion molecule requirements for neutrophil recruitment. | en_US |
dc.format.extent | 234987 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Birkhäuser Verlag; Birkhäuser Verlag, Basel, ; Springer Science+Business Media | en_US |
dc.subject.other | Legacy | en_US |
dc.subject.other | Key Words: Peritonitis — Neutrophils — Inflammation — Cytokines — Rats | en_US |
dc.title | Cytokine and adhesion molecule requirements for neutrophil recruitment during glycogen-induced peritonitis | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Pharmacy and Pharmacology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, MI 48109-0602, USA, Fax +1 313 763 4782, e-mail: pward@umich.edu, US, | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, MI 48109-0602, USA, Fax +1 313 763 4782, e-mail: pward@umich.edu, US, | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, MI 48109-0602, USA, Fax +1 313 763 4782, e-mail: pward@umich.edu, US, | en_US |
dc.contributor.affiliationother | Department of Bioregulation, Osaka University Medical School, Biomedical Research Center, 2-2 Yamadaoka, Suita 565, Japan, JP, | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 9683032 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/41819/1/11-47-6-251_80470251.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/s000110050326 | en_US |
dc.identifier.source | Inflammation Research | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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