File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Inhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells
  • Basic View
  • Metadata View
  • XML View
TitleInhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells
 
AuthorsPan, NY3
Hui, WS3
Tipoe, GL2
Taylor, GW1
Leung, RYH3
Lam, WK3
Tsang, KWT3
Mak, JCW3
 
KeywordsBronchiectasis
Dexamethasone
Fluticasone
Interleukin-8
Pseudomonas aeruginosa pyocyanin
 
Issue Date2006
 
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
 
CitationRespiratory Medicine, 2006, v. 100 n. 9, p. 1614-1622 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.rmed.2005.12.003
 
AbstractAirway epithelial cells are the first targets of environmental stimuli and local cytokines. Pyocyanin-induced synergism with interleukin (IL)-1 or tumour necrosis factor (TNF) in triggering IL-8 release has been documented previously. In this study, IL-8 mRNA and protein expression were examined in cultured human bronchial epithelial cells (BEAS-2B) stimulated with pyocyanin alone, and in combination with IL-1β or phorbol 12,13-dibutyrate (PDBu) in the absence and presence of a group of glucocorticoids. IL-8 mRNA was measured by RT-PCR, and IL-8 protein by ELISA (cell supernatants). Pyocyanin alone produced no increase in IL-8 mRNA and release. However, pyocyanin upregulated the stimulatory effect of IL-1β or PDBu on the release of IL-8 in a dose-dependent manner. The stimulatory effect of pyocyanin on the IL-1β- or PDBu-stimulated IL-8 release was reduced in the presence of dexamethasone, budesonide, and fluticasone. Budesonide and fluticasone were 10-fold more potent than dexamethasone. The protein kinase C (PKC) inhibitor, Go6976, also significantly reduced the stimulatory effect of pyocyanin on IL-1β, and PDBu increased IL-8 release. In conclusion, this study shows that PKC signal pathway seems to be involved in the pyocyanin-mediated upregulation of the IL-1β and PDBu-induced IL-8 release in BEAS-2B cells. These findings suggest that a vicious cycle perpetuating inflammation may exist in the biologic milieu of bronchiectatic patients infected with Pseudomonas aeruginosa due to the production of pyocyanin. The priming action of pyocyanin appears to be blocked by glucocorticoids, thus providing in vitro data in support of the clinical efficacy of inhaled glucocorticoids as anti-inflammatory drugs. © 2006 Elsevier Ltd. All rights reserved.
 
ISSN0954-6111
2012 Impact Factor: 2.585
2012 SCImago Journal Rankings: 1.055
 
DOIhttp://dx.doi.org/10.1016/j.rmed.2005.12.003
 
ISI Accession Number IDWOS:000239833900017
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorPan, NY
 
dc.contributor.authorHui, WS
 
dc.contributor.authorTipoe, GL
 
dc.contributor.authorTaylor, GW
 
dc.contributor.authorLeung, RYH
 
dc.contributor.authorLam, WK
 
dc.contributor.authorTsang, KWT
 
dc.contributor.authorMak, JCW
 
dc.date.accessioned2010-09-06T05:59:07Z
 
dc.date.available2010-09-06T05:59:07Z
 
dc.date.issued2006
 
dc.description.abstractAirway epithelial cells are the first targets of environmental stimuli and local cytokines. Pyocyanin-induced synergism with interleukin (IL)-1 or tumour necrosis factor (TNF) in triggering IL-8 release has been documented previously. In this study, IL-8 mRNA and protein expression were examined in cultured human bronchial epithelial cells (BEAS-2B) stimulated with pyocyanin alone, and in combination with IL-1β or phorbol 12,13-dibutyrate (PDBu) in the absence and presence of a group of glucocorticoids. IL-8 mRNA was measured by RT-PCR, and IL-8 protein by ELISA (cell supernatants). Pyocyanin alone produced no increase in IL-8 mRNA and release. However, pyocyanin upregulated the stimulatory effect of IL-1β or PDBu on the release of IL-8 in a dose-dependent manner. The stimulatory effect of pyocyanin on the IL-1β- or PDBu-stimulated IL-8 release was reduced in the presence of dexamethasone, budesonide, and fluticasone. Budesonide and fluticasone were 10-fold more potent than dexamethasone. The protein kinase C (PKC) inhibitor, Go6976, also significantly reduced the stimulatory effect of pyocyanin on IL-1β, and PDBu increased IL-8 release. In conclusion, this study shows that PKC signal pathway seems to be involved in the pyocyanin-mediated upregulation of the IL-1β and PDBu-induced IL-8 release in BEAS-2B cells. These findings suggest that a vicious cycle perpetuating inflammation may exist in the biologic milieu of bronchiectatic patients infected with Pseudomonas aeruginosa due to the production of pyocyanin. The priming action of pyocyanin appears to be blocked by glucocorticoids, thus providing in vitro data in support of the clinical efficacy of inhaled glucocorticoids as anti-inflammatory drugs. © 2006 Elsevier Ltd. All rights reserved.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationRespiratory Medicine, 2006, v. 100 n. 9, p. 1614-1622 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.rmed.2005.12.003
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.rmed.2005.12.003
 
dc.identifier.epage1622
 
dc.identifier.hkuros121431
 
dc.identifier.isiWOS:000239833900017
 
dc.identifier.issn0954-6111
2012 Impact Factor: 2.585
2012 SCImago Journal Rankings: 1.055
 
dc.identifier.issue9
 
dc.identifier.openurl
 
dc.identifier.pmid16448811
 
dc.identifier.scopuseid_2-s2.0-33746192142
 
dc.identifier.spage1614
 
dc.identifier.urihttp://hdl.handle.net/10722/67880
 
dc.identifier.volume100
 
dc.languageeng
 
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofRespiratory Medicine
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAndrostadienes - pharmacology
 
dc.subject.meshAnti-Inflammatory Agents - pharmacology
 
dc.subject.meshBronchi - cytology - drug effects - metabolism
 
dc.subject.meshBudesonide - pharmacology
 
dc.subject.meshDexamethasone - pharmacology
 
dc.subject.meshEnzyme-Linked Immunosorbent Assay
 
dc.subject.meshEpithelial Cells - drug effects - metabolism
 
dc.subject.meshGlucocorticoids - pharmacology
 
dc.subject.meshHumans
 
dc.subject.meshInterleukin-1 - pharmacology
 
dc.subject.meshInterleukin-8 - secretion
 
dc.subject.meshPhorbol 12,13-Dibutyrate - pharmacology
 
dc.subject.meshPolymerase Chain Reaction
 
dc.subject.meshProtein Kinase C - drug effects - metabolism
 
dc.subject.meshPyocyanine - pharmacology
 
dc.subject.meshRNA, Messenger - drug effects - metabolism
 
dc.subjectBronchiectasis
 
dc.subjectDexamethasone
 
dc.subjectFluticasone
 
dc.subjectInterleukin-8
 
dc.subjectPseudomonas aeruginosa pyocyanin
 
dc.titleInhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Pan, NY</contributor.author>
<contributor.author>Hui, WS</contributor.author>
<contributor.author>Tipoe, GL</contributor.author>
<contributor.author>Taylor, GW</contributor.author>
<contributor.author>Leung, RYH</contributor.author>
<contributor.author>Lam, WK</contributor.author>
<contributor.author>Tsang, KWT</contributor.author>
<contributor.author>Mak, JCW</contributor.author>
<date.accessioned>2010-09-06T05:59:07Z</date.accessioned>
<date.available>2010-09-06T05:59:07Z</date.available>
<date.issued>2006</date.issued>
<identifier.citation>Respiratory Medicine, 2006, v. 100 n. 9, p. 1614-1622</identifier.citation>
<identifier.issn>0954-6111</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/67880</identifier.uri>
<description.abstract>Airway epithelial cells are the first targets of environmental stimuli and local cytokines. Pyocyanin-induced synergism with interleukin (IL)-1 or tumour necrosis factor (TNF) in triggering IL-8 release has been documented previously. In this study, IL-8 mRNA and protein expression were examined in cultured human bronchial epithelial cells (BEAS-2B) stimulated with pyocyanin alone, and in combination with IL-1&#946; or phorbol 12,13-dibutyrate (PDBu) in the absence and presence of a group of glucocorticoids. IL-8 mRNA was measured by RT-PCR, and IL-8 protein by ELISA (cell supernatants). Pyocyanin alone produced no increase in IL-8 mRNA and release. However, pyocyanin upregulated the stimulatory effect of IL-1&#946; or PDBu on the release of IL-8 in a dose-dependent manner. The stimulatory effect of pyocyanin on the IL-1&#946;- or PDBu-stimulated IL-8 release was reduced in the presence of dexamethasone, budesonide, and fluticasone. Budesonide and fluticasone were 10-fold more potent than dexamethasone. The protein kinase C (PKC) inhibitor, Go6976, also significantly reduced the stimulatory effect of pyocyanin on IL-1&#946;, and PDBu increased IL-8 release. In conclusion, this study shows that PKC signal pathway seems to be involved in the pyocyanin-mediated upregulation of the IL-1&#946; and PDBu-induced IL-8 release in BEAS-2B cells. These findings suggest that a vicious cycle perpetuating inflammation may exist in the biologic milieu of bronchiectatic patients infected with Pseudomonas aeruginosa due to the production of pyocyanin. The priming action of pyocyanin appears to be blocked by glucocorticoids, thus providing in vitro data in support of the clinical efficacy of inhaled glucocorticoids as anti-inflammatory drugs. &#169; 2006 Elsevier Ltd. All rights reserved.</description.abstract>
<language>eng</language>
<publisher>Elsevier Ltd. The Journal&apos;s web site is located at http://www.elsevier.com/locate/rmed</publisher>
<relation.ispartof>Respiratory Medicine</relation.ispartof>
<subject>Bronchiectasis</subject>
<subject>Dexamethasone</subject>
<subject>Fluticasone</subject>
<subject>Interleukin-8</subject>
<subject>Pseudomonas aeruginosa pyocyanin</subject>
<subject.mesh>Androstadienes - pharmacology</subject.mesh>
<subject.mesh>Anti-Inflammatory Agents - pharmacology</subject.mesh>
<subject.mesh>Bronchi - cytology - drug effects - metabolism</subject.mesh>
<subject.mesh>Budesonide - pharmacology</subject.mesh>
<subject.mesh>Dexamethasone - pharmacology</subject.mesh>
<subject.mesh>Enzyme-Linked Immunosorbent Assay</subject.mesh>
<subject.mesh>Epithelial Cells - drug effects - metabolism</subject.mesh>
<subject.mesh>Glucocorticoids - pharmacology</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Interleukin-1 - pharmacology</subject.mesh>
<subject.mesh>Interleukin-8 - secretion</subject.mesh>
<subject.mesh>Phorbol 12,13-Dibutyrate - pharmacology</subject.mesh>
<subject.mesh>Polymerase Chain Reaction</subject.mesh>
<subject.mesh>Protein Kinase C - drug effects - metabolism</subject.mesh>
<subject.mesh>Pyocyanine - pharmacology</subject.mesh>
<subject.mesh>RNA, Messenger - drug effects - metabolism</subject.mesh>
<title>Inhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0954-6111&amp;volume=100&amp;issue=9&amp;spage=1614&amp;epage=1622&amp;date=2006&amp;atitle=Inhibition+of+pyocyanin-potentiated+IL-8+release+by+steroids+in+bronchial+epithelial+cells</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1016/j.rmed.2005.12.003</identifier.doi>
<identifier.pmid>16448811</identifier.pmid>
<identifier.scopus>eid_2-s2.0-33746192142</identifier.scopus>
<identifier.hkuros>121431</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-33746192142&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>100</identifier.volume>
<identifier.issue>9</identifier.issue>
<identifier.spage>1614</identifier.spage>
<identifier.epage>1622</identifier.epage>
<identifier.isi>WOS:000239833900017</identifier.isi>
<publisher.place>United Kingdom</publisher.place>
</item>
Author Affiliations
  1. UCL
  2. The University of Hong Kong
  3. Laboratory Block