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Article: Prophylactic uses of integrin CD18-βA peptide in a murine polymicrobial peritonitis model

TitleProphylactic uses of integrin CD18-βA peptide in a murine polymicrobial peritonitis model
Authors
KeywordsBacterial endotoxin
Biotherapeutic peptide
Inflammation
Integrin CD18
Issue Date2010
PublisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htm
Citation
World Journal Of Gastroenterology, 2010, v. 16 n. 21, p. 2648-2656 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/144490
ISSN
2015 Impact Factor: 2.787
2015 SCImago Journal Rankings: 1.076
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong Kong
National University of Singapore
NMRC
Funding Information:

Supported by Research Grants Council of Hong Kong, National University of Singapore and NMRC

References

 

DC FieldValueLanguage
dc.contributor.authorWong, KFen_HK
dc.contributor.authorWo, Jen_HK
dc.contributor.authorHo, Den_HK
dc.contributor.authorPoon, RTen_HK
dc.contributor.authorCasasnovas, JMen_HK
dc.contributor.authorLuk, JMen_HK
dc.date.accessioned2012-02-03T03:58:57Z-
dc.date.available2012-02-03T03:58:57Z-
dc.date.issued2010en_HK
dc.identifier.citationWorld Journal Of Gastroenterology, 2010, v. 16 n. 21, p. 2648-2656en_HK
dc.identifier.issn1007-9327en_HK
dc.identifier.urihttp://hdl.handle.net/10722/144490-
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.en_HK
dc.languageeng-
dc.publisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htmen_HK
dc.relation.ispartofWorld Journal of Gastroenterologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectBacterial endotoxinen_HK
dc.subjectBiotherapeutic peptideen_HK
dc.subjectInflammationen_HK
dc.subjectIntegrin CD18en_HK
dc.subject.meshAntigens, CD18 - therapeutic use-
dc.subject.meshEndotoxins - antagonists and inhibitors - blood-
dc.subject.meshPeptides - therapeutic use-
dc.subject.meshPeritonitis - blood - microbiology - mortality - prevention and control-
dc.subject.meshSepsis - blood - microbiology - mortality - prevention and control-
dc.titleProphylactic uses of integrin CD18-βA peptide in a murine polymicrobial peritonitis modelen_HK
dc.typeArticleen_HK
dc.identifier.emailPoon, RT: poontp@hkucc.hku.hken_HK
dc.identifier.emailLuk, JM: jmluk@hkucc.hku.hken_HK
dc.identifier.authorityPoon, RT=rp00446en_HK
dc.identifier.authorityLuk, JM=rp00349en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3748/wjg.v16.i21.2648en_HK
dc.identifier.pmid20518087-
dc.identifier.pmcidPMC2880778-
dc.identifier.scopuseid_2-s2.0-77953495377en_HK
dc.identifier.hkuros170838-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77953495377&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue21en_HK
dc.identifier.spage2648en_HK
dc.identifier.epage2656en_HK
dc.identifier.isiWOS:000278519300011-
dc.publisher.placeChinaen_HK
dc.identifier.scopusauthoridWong, KF=35081410800en_HK
dc.identifier.scopusauthoridWo, J=7003466728en_HK
dc.identifier.scopusauthoridHo, D=7402971906en_HK
dc.identifier.scopusauthoridPoon, RT=7103097223en_HK
dc.identifier.scopusauthoridCasasnovas, JM=7004669758en_HK
dc.identifier.scopusauthoridLuk, JM=7006777791en_HK

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