File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Blockage of serotonin receptor 2 attenuates cigarette-induced IL-8 release in human bronchial epithelial cells

TitleBlockage of serotonin receptor 2 attenuates cigarette-induced IL-8 release in human bronchial epithelial cells
Authors
KeywordsMedical sciences
Respiratory diseases
Issue Date2010
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
The 2010 International Conference of the American Thoracic Society (ATS), New Orleans, LA., 14-19 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2010, v. 181 (Meeting Abstracts), abstract no. A1399 How to Cite?
Abstract
INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airway limitation together with abnormal inflammation in the lung. Cigarette smoke (CS) is one of the major causes of this disease, involving the induction of inflammatory responses in the airway with increase in pro-inflammatory cytokines, i.e. interleukin-8 (IL-8). Increased systemic serotonin (5-HT) level in non-smokers after inhaling cigarette smoke (Clin Investig 1992;70:201-204) and improved lung function in COPD patients after selective serotonin receptor 2 antagonist, ketanserin (Chest 1990;97:901-905), suggest the involvement of serotoninergic system in COPD. Recently, 5-HTR2 has been found to be expressed in human lung epithelial cells and exposure to 5-HT or R-(-)-DOI-hydrochloride (DOI), a selective 5-HTR2 agonist, elevated IL-8 release (Am J Respir Cell Mol Biol 2007;36:85-93). We therefore hypothesize that serotonin is involved in CS-induced IL-8 release via activation of 5-HTR2 in human bronchial epithelial cells. The present study aims at investigating the mechanisms on how CS modulates 5-HT, leading to elevated IL-8 release in BEAS-2B cells. METHODS: Expression of 5-HTR2 subtypes and IL-8 mRNA was examined by RT-PCR. IL-8 release was determined by ELISA. Activation of MAPK pathway was assessed by Western-blot. RESULTS: We confirmed the mRNA expression of 5-HTR2 subtype in BEAS-2B cells. After exposure to CS or 5-HT, the mRNA expression as well as the release of IL-8 was elevated in parallel with the increased expression of phosphorylated ERK1/2 and p38 but not JNK. Ketanserin was found to suppress CS-induced IL-8 release by inhibiting ERK1/2 and p38 activation. CONCLUSION: These data suggest that 5-HTR2 may be involved in CS-induced IL-8 release via activation of ERK1/2 and p38 pathways in BEAS-2B cells.
DescriptionThematic Poster Session: Poster Presentation [A36] - Inflammation and the Airway Epithelium
Persistent Identifierhttp://hdl.handle.net/10722/126802
ISSN
2013 Impact Factor: 11.986

 

DC FieldValueLanguage
dc.contributor.authorLau, WKWen_HK
dc.contributor.authorLaw, ACKen_HK
dc.contributor.authorIp, MSMen_HK
dc.contributor.authorMak, JCWen_HK
dc.date.accessioned2010-10-31T12:49:21Z-
dc.date.available2010-10-31T12:49:21Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 2010 International Conference of the American Thoracic Society (ATS), New Orleans, LA., 14-19 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2010, v. 181 (Meeting Abstracts), abstract no. A1399en_HK
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/126802-
dc.descriptionThematic Poster Session: Poster Presentation [A36] - Inflammation and the Airway Epithelium-
dc.description.abstractINTRODUCTION: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airway limitation together with abnormal inflammation in the lung. Cigarette smoke (CS) is one of the major causes of this disease, involving the induction of inflammatory responses in the airway with increase in pro-inflammatory cytokines, i.e. interleukin-8 (IL-8). Increased systemic serotonin (5-HT) level in non-smokers after inhaling cigarette smoke (Clin Investig 1992;70:201-204) and improved lung function in COPD patients after selective serotonin receptor 2 antagonist, ketanserin (Chest 1990;97:901-905), suggest the involvement of serotoninergic system in COPD. Recently, 5-HTR2 has been found to be expressed in human lung epithelial cells and exposure to 5-HT or R-(-)-DOI-hydrochloride (DOI), a selective 5-HTR2 agonist, elevated IL-8 release (Am J Respir Cell Mol Biol 2007;36:85-93). We therefore hypothesize that serotonin is involved in CS-induced IL-8 release via activation of 5-HTR2 in human bronchial epithelial cells. The present study aims at investigating the mechanisms on how CS modulates 5-HT, leading to elevated IL-8 release in BEAS-2B cells. METHODS: Expression of 5-HTR2 subtypes and IL-8 mRNA was examined by RT-PCR. IL-8 release was determined by ELISA. Activation of MAPK pathway was assessed by Western-blot. RESULTS: We confirmed the mRNA expression of 5-HTR2 subtype in BEAS-2B cells. After exposure to CS or 5-HT, the mRNA expression as well as the release of IL-8 was elevated in parallel with the increased expression of phosphorylated ERK1/2 and p38 but not JNK. Ketanserin was found to suppress CS-induced IL-8 release by inhibiting ERK1/2 and p38 activation. CONCLUSION: These data suggest that 5-HTR2 may be involved in CS-induced IL-8 release via activation of ERK1/2 and p38 pathways in BEAS-2B cells.-
dc.languageengen_HK
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org-
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicine-
dc.subjectMedical sciences-
dc.subjectRespiratory diseases-
dc.titleBlockage of serotonin receptor 2 attenuates cigarette-induced IL-8 release in human bronchial epithelial cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1073-449X&volume=181 &issue=Meeting Abstracts, abstract no. A1399&spage=&epage=&date=2010&atitle=Blockage+of+serotonin+receptor+2+attenuates+cigarette-induced+IL-8+release+in+human+bronchial+epithelial+cells-
dc.identifier.emailLau, WKW: waylau@gmail.comen_HK
dc.identifier.emailLaw, ACK: acklaw@HKUCC-COM.hku.hken_HK
dc.identifier.emailIp, MSM: msmip@hku.hken_HK
dc.identifier.emailMak, JCW: judymak@HKUCC.hku.hken_HK
dc.identifier.authorityLaw, ACK=rp00262en_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.identifier.hkuros171675en_HK
dc.identifier.hkuros171727-
dc.identifier.volume181-
dc.identifier.issueMeeting Abstracts-
dc.description.otherThe 2010 International Conference of the American Thoracic Society (ATS), New Orleans, LA., 14-19 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2010, v. 181 (Meeting Abstracts), abstract no. A1399-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats