Please use this identifier to cite or link to this item: https://doi.org/10.3748/wjg.v16.i21.2648
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dc.titleProphylactic uses of integrin CD18-βA peptide in a murine polymicrobial peritonitis model
dc.contributor.authorWong, K.-F.
dc.contributor.authorWo, J.
dc.contributor.authorHo, D.
dc.contributor.authorPoon, R.T.
dc.contributor.authorCasasnovas, J.M.
dc.contributor.authorLuk, J.M.
dc.date.accessioned2014-11-26T10:00:04Z
dc.date.available2014-11-26T10:00:04Z
dc.date.issued2010-06-07
dc.identifier.citationWong, K.-F., Wo, J., Ho, D., Poon, R.T., Casasnovas, J.M., Luk, J.M. (2010-06-07). Prophylactic uses of integrin CD18-βA peptide in a murine polymicrobial peritonitis model. World Journal of Gastroenterology 16 (21) : 2648-2656. ScholarBank@NUS Repository. https://doi.org/10.3748/wjg.v16.i21.2648
dc.identifier.issn10079327
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/110771
dc.description.abstractAim: To evaluate the prophylactic properties of integrin CD18-βA peptide in a murine model of abdominal polymicrobial peritonitis and sepsis. Methods: Bacterial sepsis was induced in Institute of Cancer Research (ICR) mice by cecal ligation and puncture (CLP) surgery. Inflicted mice were then injected with either sterile saline or CD18-βA peptide intraperi-toneally at 2 h after surgery, and were sacrifced at 12 and 24 h after surgery. Blood samples were immediately collected, and analyzed for endotoxin activity and tumor necrosis factor (TNF)-α and interleukin (IL)-6. Lungs and liver were studied for CD45+ leukocyte and CD3 mRNA content. Pulmonary expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM) and E-selectin was also determined. Results: Intraperitoneal injection of CD18-βA peptide signifcantly suppressed circulating endotoxin activity (P < 0.01) at 24 h, as well as serum levels of TNF-α (P < 0.05 at 12 and 24 h) and IL-6 (P < 0.01 at 12 h, P < 0.05 at 24 h) in CLP-inflicted mice. CD18-βA peptide also abrogated leukocyte infiltration into liver and lungs as unveiled by reduced CD45+ leukocyte and CD3 mRNA contents. Furthermore, the peptide significantly reduced pulmonary expression of VCAM (P < 0.01 at 12 h, P < 0.001 at 24 h), E-selectin (P < 0.01 at 12 and 24 h), and ICAM-1 (P < 0.01 at 12 h, P < 0.001 at 24 h). These actions of CD18-βA peptide collectively protected septic mice against lethality (P < 0.01). Conclusion: CD18-βA peptide is a potent endotoxin antagonist that can protect surgical patients against sepsis-associated lethality. © 2010 Baishideng. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.3748/wjg.v16.i21.2648
dc.sourceScopus
dc.subjectBacterial endotoxin
dc.subjectBiotherapeutic peptide
dc.subjectInflammation
dc.subjectIntegrin CD18
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.3748/wjg.v16.i21.2648
dc.description.sourcetitleWorld Journal of Gastroenterology
dc.description.volume16
dc.description.issue21
dc.description.page2648-2656
dc.description.codenWJGAF
dc.identifier.isiut000278519300011
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