Differential regulation of neurotrophin expression in human bronchial smooth muscle cells
<p>Abstract</p> <p>Background</p> <p>Human bronchial smooth muscle cells (HBSMC) may regulate airway inflammation by secreting cytokines, chemokines and growth factors. The neurotrophins, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and...
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| Format: | Article |
| Language: | English |
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BMC
2006-01-01
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| Series: | Respiratory Research |
| Online Access: | http://respiratory-research.com/content/7/1/18 |
| _version_ | 1811284451470082048 |
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| author | Olgart Höglund Caroline Eklund Anders Grunewald Johan Kemi Cecilia |
| author_facet | Olgart Höglund Caroline Eklund Anders Grunewald Johan Kemi Cecilia |
| author_sort | Olgart Höglund Caroline |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>Human bronchial smooth muscle cells (HBSMC) may regulate airway inflammation by secreting cytokines, chemokines and growth factors. The neurotrophins, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), have been shown to be elevated during airway inflammation and evoke airway hyperresponsiveness. We studied if HBSMC may be a source of NGF, BDNF and NT-3, and if so, how inflammatory cytokines may influence their production.</p> <p>Methods</p> <p>Basal and cytokine (IL-1β, IFN-γ, IL-4)-stimulated neurotrophin expression in HBSMC cultured <it>in vitro </it>was quantified. The mRNA expression was quantified by real-time RT-PCR and the protein secretion into the cell culture medium by ELISA.</p> <p>Results</p> <p>We observed a constitutive NGF, BDNF and NT-3 expression. IL-1β stimulated a transient increase of NGF, while the increase of BDNF had a later onset and was more sustained. COX-inhibitors (indomethacin and NS-398) markedly decreased IL-1β-stimulated secretion of BDNF, but not IL-1β-stimulated NGF secretion. IFN-γ increased NGF expression, down-regulated BDNF expression and synergistically enhanced IL-1β-stimulated NGF expression. In contrast, IL-4 had no effect on basal NGF and BDNF expression, but decreased IL-1β-stimulated NGF expression. NT-3 was not altered by the tested cytokines.</p> <p>Conclusion</p> <p>Taken together, our data indicate that, in addition to the contractile capacity, HBSMC can express NGF, BDNF and NT-3. The expression of these neurotrophins may be differently regulated by inflammatory cytokines, suggesting a dynamic interplay that might have a potential role in airway inflammation.</p> |
| first_indexed | 2024-04-13T02:29:46Z |
| format | Article |
| id | doaj.art-d3e9115a02c149ff9d738b467d9d3772 |
| institution | Directory Open Access Journal |
| issn | 1465-9921 |
| language | English |
| last_indexed | 2024-04-13T02:29:46Z |
| publishDate | 2006-01-01 |
| publisher | BMC |
| record_format | Article |
| series | Respiratory Research |
| spelling | doaj.art-d3e9115a02c149ff9d738b467d9d37722022-12-22T03:06:39ZengBMCRespiratory Research1465-99212006-01-01711810.1186/1465-9921-7-18Differential regulation of neurotrophin expression in human bronchial smooth muscle cellsOlgart Höglund CarolineEklund AndersGrunewald JohanKemi Cecilia<p>Abstract</p> <p>Background</p> <p>Human bronchial smooth muscle cells (HBSMC) may regulate airway inflammation by secreting cytokines, chemokines and growth factors. The neurotrophins, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), have been shown to be elevated during airway inflammation and evoke airway hyperresponsiveness. We studied if HBSMC may be a source of NGF, BDNF and NT-3, and if so, how inflammatory cytokines may influence their production.</p> <p>Methods</p> <p>Basal and cytokine (IL-1β, IFN-γ, IL-4)-stimulated neurotrophin expression in HBSMC cultured <it>in vitro </it>was quantified. The mRNA expression was quantified by real-time RT-PCR and the protein secretion into the cell culture medium by ELISA.</p> <p>Results</p> <p>We observed a constitutive NGF, BDNF and NT-3 expression. IL-1β stimulated a transient increase of NGF, while the increase of BDNF had a later onset and was more sustained. COX-inhibitors (indomethacin and NS-398) markedly decreased IL-1β-stimulated secretion of BDNF, but not IL-1β-stimulated NGF secretion. IFN-γ increased NGF expression, down-regulated BDNF expression and synergistically enhanced IL-1β-stimulated NGF expression. In contrast, IL-4 had no effect on basal NGF and BDNF expression, but decreased IL-1β-stimulated NGF expression. NT-3 was not altered by the tested cytokines.</p> <p>Conclusion</p> <p>Taken together, our data indicate that, in addition to the contractile capacity, HBSMC can express NGF, BDNF and NT-3. The expression of these neurotrophins may be differently regulated by inflammatory cytokines, suggesting a dynamic interplay that might have a potential role in airway inflammation.</p>http://respiratory-research.com/content/7/1/18 |
| spellingShingle | Olgart Höglund Caroline Eklund Anders Grunewald Johan Kemi Cecilia Differential regulation of neurotrophin expression in human bronchial smooth muscle cells Respiratory Research |
| title | Differential regulation of neurotrophin expression in human bronchial smooth muscle cells |
| title_full | Differential regulation of neurotrophin expression in human bronchial smooth muscle cells |
| title_fullStr | Differential regulation of neurotrophin expression in human bronchial smooth muscle cells |
| title_full_unstemmed | Differential regulation of neurotrophin expression in human bronchial smooth muscle cells |
| title_short | Differential regulation of neurotrophin expression in human bronchial smooth muscle cells |
| title_sort | differential regulation of neurotrophin expression in human bronchial smooth muscle cells |
| url | http://respiratory-research.com/content/7/1/18 |
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