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Article: Upregulation of ICAM-1 expression in bronchial epithelial cells by airway secretions in bronchiectasis

TitleUpregulation of ICAM-1 expression in bronchial epithelial cells by airway secretions in bronchiectasis
Authors
KeywordsBronchial epithelial cells
Bronchiectasis
Drug modulation
Intercellular cell adhesion molecule
Tumor necrosis factor-α
Issue Date2008
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
Citation
Respiratory Medicine, 2008, v. 102 n. 2, p. 287-298 How to Cite?
AbstractThe airway epithelium participates in chronic airway inflammation by expressing adhesion molecules that mediate the transmigration of neutrophils into the inflamed airways. We hypothesize that, in patients with bronchiectasis, cytokines in their bronchial secretions enhance the expression of intercellular cell adhesion molecule (ICAM-1) in the bronchial epithelium and thus contribute to sustained recruitment of neutrophils into the inflamed airways. In the present study, we investigated the effect of bronchial secretions on the regulation of ICAM-1 in bronchial epithelial cells, and its modulation by pharmacologic agents. The expression of ICAM-1 mRNA and protein in human bronchial epithelial cells upon exposure to sputum sol from subjects with bronchiectasis were evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and ELISA, respectively. Modulating effects of dexamethasone, ibuprofen, MK-663 or triptolide on ICAM-1 regulation were investigated in vitro. We demonstrated that changes in ICAM-1 expression correlated with levels of TNF-α in the sputum sol, and treatment of sol samples with TNF-α antibodies attenuated both the increase in ICAM-1 mRNA and protein. The role of TNF-α was further demonstrated when TNF-α elicited dose dependent increase in ICAM-1 expression. The sputum effect could also be suppressed dose-dependently by pre-incubation of bronchial epithelial cells with dexamethasone, ibuprofen, MK-663 or triptolide. Evidence is thus provided for the upregulation of bronchial epithelial ICAM-1 expression by airway secretions in bronchiectasis and a specific role for TNF-α in the secretions. The success of drug attenuation of this upregulation provides insight into possible therapeutic paradigms in the management of the disease. © 2007 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67444
ISSN
2015 Impact Factor: 3.036
2015 SCImago Journal Rankings: 1.396
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, SCHen_HK
dc.contributor.authorShum, DKYen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorMak, JCWen_HK
dc.contributor.authorLeung, ETMen_HK
dc.contributor.authorIp, MSMen_HK
dc.date.accessioned2010-09-06T05:55:11Z-
dc.date.available2010-09-06T05:55:11Z-
dc.date.issued2008en_HK
dc.identifier.citationRespiratory Medicine, 2008, v. 102 n. 2, p. 287-298en_HK
dc.identifier.issn0954-6111en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67444-
dc.description.abstractThe airway epithelium participates in chronic airway inflammation by expressing adhesion molecules that mediate the transmigration of neutrophils into the inflamed airways. We hypothesize that, in patients with bronchiectasis, cytokines in their bronchial secretions enhance the expression of intercellular cell adhesion molecule (ICAM-1) in the bronchial epithelium and thus contribute to sustained recruitment of neutrophils into the inflamed airways. In the present study, we investigated the effect of bronchial secretions on the regulation of ICAM-1 in bronchial epithelial cells, and its modulation by pharmacologic agents. The expression of ICAM-1 mRNA and protein in human bronchial epithelial cells upon exposure to sputum sol from subjects with bronchiectasis were evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and ELISA, respectively. Modulating effects of dexamethasone, ibuprofen, MK-663 or triptolide on ICAM-1 regulation were investigated in vitro. We demonstrated that changes in ICAM-1 expression correlated with levels of TNF-α in the sputum sol, and treatment of sol samples with TNF-α antibodies attenuated both the increase in ICAM-1 mRNA and protein. The role of TNF-α was further demonstrated when TNF-α elicited dose dependent increase in ICAM-1 expression. The sputum effect could also be suppressed dose-dependently by pre-incubation of bronchial epithelial cells with dexamethasone, ibuprofen, MK-663 or triptolide. Evidence is thus provided for the upregulation of bronchial epithelial ICAM-1 expression by airway secretions in bronchiectasis and a specific role for TNF-α in the secretions. The success of drug attenuation of this upregulation provides insight into possible therapeutic paradigms in the management of the disease. © 2007 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmeden_HK
dc.relation.ispartofRespiratory Medicineen_HK
dc.subjectBronchial epithelial cellsen_HK
dc.subjectBronchiectasisen_HK
dc.subjectDrug modulationen_HK
dc.subjectIntercellular cell adhesion moleculeen_HK
dc.subjectTumor necrosis factor-αen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAnti-Inflammatory Agents - pharmacologyen_HK
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - pharmacologyen_HK
dc.subject.meshBronchi - immunologyen_HK
dc.subject.meshBronchiectasis - immunologyen_HK
dc.subject.meshCyclooxygenase 2 Inhibitors - pharmacologyen_HK
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_HK
dc.subject.meshEpithelial Cells - drug effects - immunologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunosuppressive Agents - pharmacologyen_HK
dc.subject.meshIntercellular Adhesion Molecule-1 - analysisen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshRNA, Messenger - analysisen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTumor Necrosis Factor-alpha - analysis - pharmacologyen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleUpregulation of ICAM-1 expression in bronchial epithelial cells by airway secretions in bronchiectasisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0954-6111&volume=102&spage=287&epage=298&date=2008&atitle=Upregulation+of+ICAM-1+expression+in+bronchial+epithelial+cells+by+airway+secretions+in+bronchiectasisen_HK
dc.identifier.emailShum, DKY:shumdkhk@hkucc.hku.hken_HK
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_HK
dc.identifier.emailMak, JCW:judymak@hku.hken_HK
dc.identifier.emailIp, MSM:msmip@hku.hken_HK
dc.identifier.authorityShum, DKY=rp00321en_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.rmed.2007.08.013en_HK
dc.identifier.pmid17931847-
dc.identifier.scopuseid_2-s2.0-37349034982en_HK
dc.identifier.hkuros141233en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37349034982&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume102en_HK
dc.identifier.issue2en_HK
dc.identifier.spage287en_HK
dc.identifier.epage298en_HK
dc.identifier.isiWOS:000252809500014-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, SCH=35261745200en_HK
dc.identifier.scopusauthoridShum, DKY=7004824447en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridMak, JCW=7103323094en_HK
dc.identifier.scopusauthoridLeung, ETM=27168491300en_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK

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