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Article: Tumor necrosis factor-induced interleukin-8 expression in cultured human airway epithelial cells

TitleTumor necrosis factor-induced interleukin-8 expression in cultured human airway epithelial cells
Authors
Issue Date1994
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/
Citation
American Journal Of Physiology - Lung Cellular And Molecular Physiology, 1994, v. 267 n. 4 11-4, p. L398-L405 How to Cite?
AbstractThe effects of tumor necrosis factor-α (TNF-α) on interleukin-8 (IL-8) expression and generation were examined in primary cultured human airway epithelial cells (HAEC) and a human lung epithelial cell line (A549). TNF-α increased IL-8 mRNA and protein expression in HAEC in a concentration- and time-dependent manner and these effects were inhibited by dexamethasone (1 μM). There was no change in the stability of IL-8 mRNA, and a nuclear run- on assay confirmed that TNF-α increased IL-8 gene transcription. TNF-α- induced IL-8 mRNA expression showed a biphasic response in HAEC, with an early increase at 2 h followed by a sustained increase from 8 h, which was abolished by the addition of cycloheximide, suggesting that the synthesis of another protein was involved. A549 cells also increased IL-8 secretion and mRNA after incubation of TNF-α, with inhibition by dexamethasone. However, A549 cells showed only an early single peak. A549 cells showed a 250-fold increase in the generation of IL-8 immunoreactivity, whereas primary cultured HAEC showed only a threefold increase, suggesting that HAEC and A549 cells may respond to TNF-α in different ways. The sustained increase in IL-8 secretion due to an increase in gene transcription in response to TNF-α may be an important amplification step in inflammatory diseases of the airways.
Persistent Identifierhttp://hdl.handle.net/10722/162022
ISSN
2015 Impact Factor: 4.721
2015 SCImago Journal Rankings: 1.838
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorO Jung Kwonen_US
dc.contributor.authorAu, BTen_US
dc.contributor.authorCollins, PDen_US
dc.contributor.authorAdcock, IMen_US
dc.contributor.authorMak, JCen_US
dc.contributor.authorRobbins, RRen_US
dc.contributor.authorChung, KFen_US
dc.contributor.authorBarnes, PJen_US
dc.date.accessioned2012-09-05T05:16:43Z-
dc.date.available2012-09-05T05:16:43Z-
dc.date.issued1994en_US
dc.identifier.citationAmerican Journal Of Physiology - Lung Cellular And Molecular Physiology, 1994, v. 267 n. 4 11-4, p. L398-L405en_US
dc.identifier.issn1040-0605en_US
dc.identifier.urihttp://hdl.handle.net/10722/162022-
dc.description.abstractThe effects of tumor necrosis factor-α (TNF-α) on interleukin-8 (IL-8) expression and generation were examined in primary cultured human airway epithelial cells (HAEC) and a human lung epithelial cell line (A549). TNF-α increased IL-8 mRNA and protein expression in HAEC in a concentration- and time-dependent manner and these effects were inhibited by dexamethasone (1 μM). There was no change in the stability of IL-8 mRNA, and a nuclear run- on assay confirmed that TNF-α increased IL-8 gene transcription. TNF-α- induced IL-8 mRNA expression showed a biphasic response in HAEC, with an early increase at 2 h followed by a sustained increase from 8 h, which was abolished by the addition of cycloheximide, suggesting that the synthesis of another protein was involved. A549 cells also increased IL-8 secretion and mRNA after incubation of TNF-α, with inhibition by dexamethasone. However, A549 cells showed only an early single peak. A549 cells showed a 250-fold increase in the generation of IL-8 immunoreactivity, whereas primary cultured HAEC showed only a threefold increase, suggesting that HAEC and A549 cells may respond to TNF-α in different ways. The sustained increase in IL-8 secretion due to an increase in gene transcription in response to TNF-α may be an important amplification step in inflammatory diseases of the airways.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Lung Cellular and Molecular Physiologyen_US
dc.subject.meshBronchi - Cytology - Metabolismen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCycloheximide - Pharmacologyen_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshEpithelial Cellsen_US
dc.subject.meshEpithelium - Metabolismen_US
dc.subject.meshHalf-Lifeen_US
dc.subject.meshHumansen_US
dc.subject.meshInterleukin-8 - Genetics - Metabolismen_US
dc.subject.meshLung - Cytology - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshTrachea - Cytology - Metabolismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Pharmacologyen_US
dc.titleTumor necrosis factor-induced interleukin-8 expression in cultured human airway epithelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailMak, JC:judymak@hku.hken_US
dc.identifier.authorityMak, JC=rp00352en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7943343-
dc.identifier.scopuseid_2-s2.0-0027946605en_US
dc.identifier.volume267en_US
dc.identifier.issue4 11-4en_US
dc.identifier.spageL398en_US
dc.identifier.epageL405en_US
dc.identifier.isiWOS:A1994PW55500006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridO Jung Kwon=7409727112en_US
dc.identifier.scopusauthoridAu, BT=7003656019en_US
dc.identifier.scopusauthoridCollins, PD=7402501065en_US
dc.identifier.scopusauthoridAdcock, IM=7007066538en_US
dc.identifier.scopusauthoridMak, JC=7103323094en_US
dc.identifier.scopusauthoridRobbins, RR=7202459895en_US
dc.identifier.scopusauthoridChung, KF=35403525000en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US

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