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postgraduate thesis: The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells

TitleThe effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells
Authors
Issue Date2013
PublisherThe University of Hong Kong (Pokfulam, Hong Kong)
Citation
Lai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422
AbstractChronic obstructive pulmonary disease (COPD) is a highly prevalent disease in the elderly. It is currently the fourth leading cause of death and will become the third by 2030. Cigarette smoke is the major cause of COPD pathogenesis, resulting from the burden of oxidants, which stimulates the production of inflammatory chemokines, leading to the influx of inflammatory cells into the airways and causing chronic inflammation. Due to lung infection by bacteria, such as Pseudomonas Aeruginosa during acute exacerbation in COPD, cigarette smoking might induce an immunosuppressive effect, which leads to bacteria colonization in the airways and further contributes to the chronic inflammation in the airway of COPD. Furthermore, cigarette smoke-induced production of reactive oxygen species (ROS) also plays an important role in the pathogenesis of COPD, however, N-acetyl-L-cysteine (NAC), which has been administered for the treatment of COPD as a mucolytic agent, also showed antioxidant and anti-inflammatory effect. The exact mechanism or cellular pathway through which cigarette smoke suppresses bacteria-induced inflammatory response and how NAC acts as an anti-inflammatory agent still remains uncertain. This study aims to investigate the effect of cigarette smoke and lipopolysaccharide (LPS) alone or in combination on the release of pro-inflammatory chemokines and to elucidate cigarette smoke-induced chemokines release in the presence and absence of NAC. Both cigarette smoke and LPS alone induced the release of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1).Cigarette smoke suppressed the LPS-induced IL-8 and MCP-1release. NAC reduced both basal and cigarette smoke-induced secretion of these inflammatory chemokines. Moreover, Western blot demonstrated that cigarette smoke activated AMPKα phosphorylation, which was suppressed with NAC pretreatment, suggesting that NAC might have inhibitory effect on the release of chemokine release via the AMPK pathway. Our current data suggests that there may be a link between ROS generation to AMPK activation and chemokine release in BEAS-2B cells.
DegreeMaster of Medical Sciences
SubjectEpithelial cells
Cigarette smoke
Endotoxins
Dept/ProgramPharmacology and Pharmacy
Persistent Identifierhttp://hdl.handle.net/10722/193537

 

DC FieldValueLanguage
dc.contributor.authorLai, Wing-yin, Joan-
dc.contributor.author賴穎賢-
dc.date.accessioned2014-01-13T23:10:35Z-
dc.date.available2014-01-13T23:10:35Z-
dc.date.issued2013-
dc.identifier.citationLai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422-
dc.identifier.urihttp://hdl.handle.net/10722/193537-
dc.description.abstractChronic obstructive pulmonary disease (COPD) is a highly prevalent disease in the elderly. It is currently the fourth leading cause of death and will become the third by 2030. Cigarette smoke is the major cause of COPD pathogenesis, resulting from the burden of oxidants, which stimulates the production of inflammatory chemokines, leading to the influx of inflammatory cells into the airways and causing chronic inflammation. Due to lung infection by bacteria, such as Pseudomonas Aeruginosa during acute exacerbation in COPD, cigarette smoking might induce an immunosuppressive effect, which leads to bacteria colonization in the airways and further contributes to the chronic inflammation in the airway of COPD. Furthermore, cigarette smoke-induced production of reactive oxygen species (ROS) also plays an important role in the pathogenesis of COPD, however, N-acetyl-L-cysteine (NAC), which has been administered for the treatment of COPD as a mucolytic agent, also showed antioxidant and anti-inflammatory effect. The exact mechanism or cellular pathway through which cigarette smoke suppresses bacteria-induced inflammatory response and how NAC acts as an anti-inflammatory agent still remains uncertain. This study aims to investigate the effect of cigarette smoke and lipopolysaccharide (LPS) alone or in combination on the release of pro-inflammatory chemokines and to elucidate cigarette smoke-induced chemokines release in the presence and absence of NAC. Both cigarette smoke and LPS alone induced the release of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1).Cigarette smoke suppressed the LPS-induced IL-8 and MCP-1release. NAC reduced both basal and cigarette smoke-induced secretion of these inflammatory chemokines. Moreover, Western blot demonstrated that cigarette smoke activated AMPKα phosphorylation, which was suppressed with NAC pretreatment, suggesting that NAC might have inhibitory effect on the release of chemokine release via the AMPK pathway. Our current data suggests that there may be a link between ROS generation to AMPK activation and chemokine release in BEAS-2B cells.-
dc.languageeng-
dc.publisherThe University of Hong Kong (Pokfulam, Hong Kong)-
dc.relation.ispartofHKU Theses Online (HKUTO)-
dc.rightsThe author retains all proprietary rights, (such as patent rights) and the right to use in future works.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.lcshEpithelial cells-
dc.subject.lcshCigarette smoke-
dc.subject.lcshEndotoxins-
dc.titleThe effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells-
dc.typePG_Thesis-
dc.identifier.hkulb5091422-
dc.description.thesisnameMaster of Medical Sciences-
dc.description.thesislevelMaster-
dc.description.thesisdisciplinePharmacology and Pharmacy-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.5353/th_b5091422-
dc.date.hkucongregation2013-

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