Intratracheal administration of endotoxin and cytokines: VIII. LPS induces E-selectin expression; anti-E-selectin and soluble E-selectin inhibit acute inflammation
dc.contributor.author | Collins, Tucker | en_US |
dc.contributor.author | Yi, Eunhee S. | en_US |
dc.contributor.author | Guo, Kaizhi | en_US |
dc.contributor.author | Williams, James H. | en_US |
dc.contributor.author | Steininger, Christina N. | en_US |
dc.contributor.author | Welply, Joseph K. | en_US |
dc.contributor.author | Keene, Jeffery L. | en_US |
dc.contributor.author | Schmuke, Jon J. | en_US |
dc.contributor.author | Ulich, Thomas R. | en_US |
dc.contributor.author | Howard, Susan C. | en_US |
dc.contributor.author | Remick, Daniel G. | en_US |
dc.contributor.author | Yin, Songmei | en_US |
dc.date.accessioned | 2006-09-11T14:55:00Z | |
dc.date.available | 2006-09-11T14:55:00Z | |
dc.date.issued | 1994-08 | en_US |
dc.identifier.citation | Ulich, Thomas R.; Howard, Susan C.; Remick, Daniel G.; Yi, Eunhee S.; Collins, Tucker; Guo, Kaizhi; Yin, Songmei; Keene, Jeffery L.; Schmuke, Jon J.; Steininger, Christina N.; Welply, Joseph K.; Williams, James H.; (1994). "Intratracheal administration of endotoxin and cytokines: VIII. LPS induces E-selectin expression; anti-E-selectin and soluble E-selectin inhibit acute inflammation." Inflammation 18(4): 389-398. <http://hdl.handle.net/2027.42/44513> | en_US |
dc.identifier.issn | 0360-3997 | en_US |
dc.identifier.issn | 1573-2576 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/44513 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7527013&dopt=citation | en_US |
dc.description.abstract | E-selectin is an inducible endothelial adhesion molecule that binds neutrophils. E-selectin mRNA is not constitutively detectable in the lungs of rats. Intratracheal injection of LPS induces pulmonary E-selectin mRNA expression at 2–4 h. Intratracheal injection of LPS followed at 2 and 4 h by intravenous injection of mouse F(ab′) 2 or F(ab′)) anti-E-selectin monoclonal antibody inhibits the emigration of neutrophils into the bronchoalveolar space at 6 h by 50–70%. TNF and IL-6 bioactivity are not decreased in bronchoalveolar lavage fluid after treatment with anti-E-selectin antibody as compared to controls, suggesting that the anti-E-selectin does not affect the magnitude of the LPS-initiated cytokine cascade. Intratracheal injection of LPS followed at 2 and 4 h by intravenous injection of soluble E-selectin inhibits neutrophilic emigration at 6 h by 64%, suggesting that endogenous soluble E-selectin shed from activated endothelium may play a role in the endogenous down-regulation of acute inflammation. E-selectin-mediated adhesion of neutrophils to endothelium appears crucial to the full development of the acute inflammation response. | en_US |
dc.format.extent | 601755 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers-Plenum Publishers; Plenum Publishing Corporation ; Springer Science+Business Media | en_US |
dc.subject.other | Medicine & Public Health | en_US |
dc.subject.other | Internal Medicine | en_US |
dc.subject.other | Pharmacology/Toxicology | en_US |
dc.subject.other | Pathology | en_US |
dc.subject.other | Rheumatology | en_US |
dc.title | Intratracheal administration of endotoxin and cytokines: VIII. LPS induces E-selectin expression; anti-E-selectin and soluble E-selectin inhibit acute inflammation | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Pathology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan School of Medicine, 48109, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Division of Glycosciences Department of Immunology and Infectious Diseases, Monsanto Corporate Research, 63137, St. Louis, Missouri | en_US |
dc.contributor.affiliationother | Department of Pathology, UC San Diego School of Medicine, 92103, San Diego, California | en_US |
dc.contributor.affiliationother | Department of Pathology, UC San Diego School of Medicine, 92103, San Diego, California | en_US |
dc.contributor.affiliationother | Department of Pathology, Brigham and Women's Hospital, 02115, Boston, Massachusetts | en_US |
dc.contributor.affiliationother | Department of Medicine, UC Irvine School of Medicine Irvine, 92717, California | en_US |
dc.contributor.affiliationother | Department of Pathology, UC San Diego School of Medicine, 92103, San Diego, California | en_US |
dc.contributor.affiliationother | Division of Glycosciences Department of Immunology and Infectious Diseases, Monsanto Corporate Research, 63137, St. Louis, Missouri | en_US |
dc.contributor.affiliationother | Division of Glycosciences Department of Immunology and Infectious Diseases, Monsanto Corporate Research, 63137, St. Louis, Missouri | en_US |
dc.contributor.affiliationother | Division of Glycosciences Department of Immunology and Infectious Diseases, Monsanto Corporate Research, 63137, St. Louis, Missouri | en_US |
dc.contributor.affiliationother | Division of Glycosciences Department of Immunology and Infectious Diseases, Monsanto Corporate Research, 63137, St. Louis, Missouri | en_US |
dc.contributor.affiliationother | Department of Medicine, UC Irvine School of Medicine Irvine, 92717, California | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 7527013 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/44513/1/10753_2005_Article_BF01534436.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF01534436 | en_US |
dc.identifier.source | Inflammation | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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