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Article: In vitro study of regulation of IL-6 production in bronchiectasis

TitleIn vitro study of regulation of IL-6 production in bronchiectasis
Authors
KeywordsBronchiectasis
Drug modulation
Interleukin-6
Issue Date2004
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
Citation
Respiratory Medicine, 2004, v. 98 n. 4, p. 334-341 How to Cite?
Abstract
Persistent airway inflammation is an important pathogenetic factor in bronchiectasis, and interleukin (IL)-6 is among the mediators implicated in regulation of inflammation in bronchiectatic airways. We postulated that airway secretion with its constituents of cytokines and enzymes would provide an environment for perpetuation of inflammation in vivo. We aimed to determine the action of sputum from patients with bronchiectasis on IL-6 production from cultured normal human bronchial epithelial (NHBE) cells and its modulation by anti-inflammatory drugs in vitro. Cultures of NHBE cells were tested with (i) sputum of bronchiectatic patients, (ii) anti-tumor necrosis factor-alpha (TNF-α) pre-treated sputum, or (iii) recombinant human (rh)-TNF-α. Alternatively, NHBE cells were incubated with one of the anti-inflammatory drugs before treatment with sputum or rh-TNF-α. IL-6 produced into the medium was assayed by ELISA. Sputum in bronchiectasis stimulated IL-6 production from NHBE cells by 1.9 times. This was largely attributable to TNF-α as pre-incubation of sputum sol with anti-TNF-α almost neutralized the sputum effect. Apart from dexamethasone, the other drugs exerted inhibitory effects on IL-6 production. Ibuprofen suppressed sputum-stimulated IL-6 production to levels above control and effect levelled off at 50-100μg/ml, contrasting the dose-dependent suppression to control level with MK-663 (0.1-10μg/ml) and to sub-control levels with triptolide (20-1000ng/ml). Our results support that sputum in bronchiectasis can stimulate IL-6 production from NHBE cells, and TNF-α is an important cytokine mediating the process. The suppressive effects observed with ibuprofen, triptolide and MK-663 warrant further study. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67571
ISSN
2013 Impact Factor: 2.917
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorHo, JCen_HK
dc.contributor.authorTipoe, Gen_HK
dc.contributor.authorZheng, Len_HK
dc.contributor.authorLeung, TMen_HK
dc.contributor.authorTsang, KWTen_HK
dc.contributor.authorShum, DKYen_HK
dc.contributor.authorLau, CSen_HK
dc.contributor.authorMak, JCWen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorIp, MSMen_HK
dc.date.accessioned2010-09-06T05:56:19Z-
dc.date.available2010-09-06T05:56:19Z-
dc.date.issued2004en_HK
dc.identifier.citationRespiratory Medicine, 2004, v. 98 n. 4, p. 334-341en_HK
dc.identifier.issn0954-6111en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67571-
dc.description.abstractPersistent airway inflammation is an important pathogenetic factor in bronchiectasis, and interleukin (IL)-6 is among the mediators implicated in regulation of inflammation in bronchiectatic airways. We postulated that airway secretion with its constituents of cytokines and enzymes would provide an environment for perpetuation of inflammation in vivo. We aimed to determine the action of sputum from patients with bronchiectasis on IL-6 production from cultured normal human bronchial epithelial (NHBE) cells and its modulation by anti-inflammatory drugs in vitro. Cultures of NHBE cells were tested with (i) sputum of bronchiectatic patients, (ii) anti-tumor necrosis factor-alpha (TNF-α) pre-treated sputum, or (iii) recombinant human (rh)-TNF-α. Alternatively, NHBE cells were incubated with one of the anti-inflammatory drugs before treatment with sputum or rh-TNF-α. IL-6 produced into the medium was assayed by ELISA. Sputum in bronchiectasis stimulated IL-6 production from NHBE cells by 1.9 times. This was largely attributable to TNF-α as pre-incubation of sputum sol with anti-TNF-α almost neutralized the sputum effect. Apart from dexamethasone, the other drugs exerted inhibitory effects on IL-6 production. Ibuprofen suppressed sputum-stimulated IL-6 production to levels above control and effect levelled off at 50-100μg/ml, contrasting the dose-dependent suppression to control level with MK-663 (0.1-10μg/ml) and to sub-control levels with triptolide (20-1000ng/ml). Our results support that sputum in bronchiectasis can stimulate IL-6 production from NHBE cells, and TNF-α is an important cytokine mediating the process. The suppressive effects observed with ibuprofen, triptolide and MK-663 warrant further study. © 2003 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.subjectBronchiectasisen_HK
dc.subjectDrug modulationen_HK
dc.subjectInterleukin-6en_HK
dc.subject.meshAnti-Inflammatory Agents - pharmacology-
dc.subject.meshBronchiectasis - metabolism-
dc.subject.meshCells, Cultured-
dc.subject.meshEpithelial Cells-
dc.subject.meshInterleukin-6 - biosynthesis-
dc.titleIn vitro study of regulation of IL-6 production in bronchiectasisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0954-6111&volume=98&issue=4&spage=334&epage=341&date=2004&atitle=In+vitro+study+of+regulation+of+IL-6+production+in+bronchiectasisen_HK
dc.identifier.emailHo, JC:jhocm@hku.hken_HK
dc.identifier.emailTipoe, G:tgeorge@hkucc.hku.hken_HK
dc.identifier.emailShum, DKY:shumdkhk@hkucc.hku.hken_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.emailMak, JCW:judymak@hku.hken_HK
dc.identifier.emailIp, MSM:msmip@hku.hken_HK
dc.identifier.authorityHo, JC=rp00258en_HK
dc.identifier.authorityTipoe, G=rp00371en_HK
dc.identifier.authorityShum, DKY=rp00321en_HK
dc.identifier.authorityLau, CS=rp01348en_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.2003.10.012en_HK
dc.identifier.pmid15072174en_HK
dc.identifier.scopuseid_2-s2.0-11144358561en_HK
dc.identifier.hkuros85890en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-11144358561&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume98en_HK
dc.identifier.issue4en_HK
dc.identifier.spage334en_HK
dc.identifier.epage341en_HK
dc.identifier.isiWOS:000220633100009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridHo, JC=7402649981en_HK
dc.identifier.scopusauthoridTipoe, G=7003550610en_HK
dc.identifier.scopusauthoridZheng, L=7403404086en_HK
dc.identifier.scopusauthoridLeung, TM=55236116600en_HK
dc.identifier.scopusauthoridTsang, KWT=7201555024en_HK
dc.identifier.scopusauthoridShum, DKY=7004824447en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK
dc.identifier.scopusauthoridMak, JCW=7103323094en_HK
dc.identifier.scopusauthoridLam, WK=7203021937en_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK

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