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Conference Paper: Blockage of serotonin receptor 2 attenuates cigarette-induced IL-8 release in human bronchial epithelial cells
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TitleBlockage of serotonin receptor 2 attenuates cigarette-induced IL-8 release in human bronchial epithelial cells
 
AuthorsLau, WKW
Law, ACK
Ip, MSM
Mak, JCW
 
KeywordsMedical sciences
Respiratory diseases
 
Issue Date2010
 
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
 
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. A1399 [How to Cite?]
 
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.
 
DescriptionThematic Poster Session: Poster Presentation [A36] - Inflammation and the Airway Epithelium
 
ISSN1073-449X
2012 Impact Factor: 11.041
2012 SCImago Journal Rankings: 4.892
 
DC FieldValue
dc.contributor.authorLau, WKW
 
dc.contributor.authorLaw, ACK
 
dc.contributor.authorIp, MSM
 
dc.contributor.authorMak, JCW
 
dc.date.accessioned2010-10-31T12:49:21Z
 
dc.date.available2010-10-31T12:49:21Z
 
dc.date.issued2010
 
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.descriptionThematic Poster Session: Poster Presentation [A36] - Inflammation and the Airway Epithelium
 
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
 
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. A1399 [How to Cite?]
 
dc.identifier.hkuros171675
 
dc.identifier.hkuros171727
 
dc.identifier.issn1073-449X
2012 Impact Factor: 11.041
2012 SCImago Journal Rankings: 4.892
 
dc.identifier.issueMeeting Abstracts
 
dc.identifier.openurl
 
dc.identifier.urihttp://hdl.handle.net/10722/126802
 
dc.identifier.volume181
 
dc.languageeng
 
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 cells
 
dc.typeConference_Paper
 
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<description.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.</description.abstract>
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