Morphine stimulates CCL2 production by human neurons
<p>Abstract</p> <p>Background</p> <p>Substances of abuse, such as opiates, have a variety of immunomodulatory properties that may influence both neuroinflammatory and neurodegenerative disease processes. The chemokine CCL2, which plays a pivotal role in the recruitment...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2006-12-01
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| Series: | Journal of Neuroinflammation |
| Online Access: | http://www.jneuroinflammation.com/content/3/1/32 |
| _version_ | 1811298506113024000 |
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| author | Sheng Wen S Hu Shuxian Rock R Bryan Peterson Phillip K |
| author_facet | Sheng Wen S Hu Shuxian Rock R Bryan Peterson Phillip K |
| author_sort | Sheng Wen S |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>Substances of abuse, such as opiates, have a variety of immunomodulatory properties that may influence both neuroinflammatory and neurodegenerative disease processes. The chemokine CCL2, which plays a pivotal role in the recruitment of inflammatory cells in the nervous system, is one of only a few chemokines produced by neurons. We hypothesized that morphine may alter expression of CCL2 by human neurons.</p> <p>Methods</p> <p>Primary neuronal cell cultures and highly purified astrocyte and microglial cell cultures were prepared from human fetal brain tissue. Cell cultures were treated with morphine, and cells were examined by RNase protection assay for mRNA. Culture supernatants were assayed by ELISA for CCL2 protein. β-funaltrexamine (β-FNA) was used to block μ-opioid receptor (MOR)s.</p> <p>Results</p> <p>Morphine upregulated CCL2 mRNA and protein in neuronal cultures in a concentration- and time-dependent fashion, but had no effect on CCL2 production in astrocyte or microglial cell cultures. Immunocytochemical analysis also demonstrated CCL2 production in morphine-stimulated neuronal cultures. The stimulatory effect of morphine was abrogated by β-FNA, indicating an MOR-mediated mechanism.</p> <p>Conclusion</p> <p>Morphine stimulates CCL2 production by human neurons via a MOR-related mechanism. This finding suggests another mechanism whereby opiates could affect neuroinflammatory responses.</p> |
| first_indexed | 2024-04-13T06:21:14Z |
| format | Article |
| id | doaj.art-bcfe9d915c594c97a0f2e3d1bd5b5c73 |
| institution | Directory Open Access Journal |
| issn | 1742-2094 |
| language | English |
| last_indexed | 2024-04-13T06:21:14Z |
| publishDate | 2006-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Neuroinflammation |
| spelling | doaj.art-bcfe9d915c594c97a0f2e3d1bd5b5c732022-12-22T02:58:39ZengBMCJournal of Neuroinflammation1742-20942006-12-01313210.1186/1742-2094-3-32Morphine stimulates CCL2 production by human neuronsSheng Wen SHu ShuxianRock R BryanPeterson Phillip K<p>Abstract</p> <p>Background</p> <p>Substances of abuse, such as opiates, have a variety of immunomodulatory properties that may influence both neuroinflammatory and neurodegenerative disease processes. The chemokine CCL2, which plays a pivotal role in the recruitment of inflammatory cells in the nervous system, is one of only a few chemokines produced by neurons. We hypothesized that morphine may alter expression of CCL2 by human neurons.</p> <p>Methods</p> <p>Primary neuronal cell cultures and highly purified astrocyte and microglial cell cultures were prepared from human fetal brain tissue. Cell cultures were treated with morphine, and cells were examined by RNase protection assay for mRNA. Culture supernatants were assayed by ELISA for CCL2 protein. β-funaltrexamine (β-FNA) was used to block μ-opioid receptor (MOR)s.</p> <p>Results</p> <p>Morphine upregulated CCL2 mRNA and protein in neuronal cultures in a concentration- and time-dependent fashion, but had no effect on CCL2 production in astrocyte or microglial cell cultures. Immunocytochemical analysis also demonstrated CCL2 production in morphine-stimulated neuronal cultures. The stimulatory effect of morphine was abrogated by β-FNA, indicating an MOR-mediated mechanism.</p> <p>Conclusion</p> <p>Morphine stimulates CCL2 production by human neurons via a MOR-related mechanism. This finding suggests another mechanism whereby opiates could affect neuroinflammatory responses.</p>http://www.jneuroinflammation.com/content/3/1/32 |
| spellingShingle | Sheng Wen S Hu Shuxian Rock R Bryan Peterson Phillip K Morphine stimulates CCL2 production by human neurons Journal of Neuroinflammation |
| title | Morphine stimulates CCL2 production by human neurons |
| title_full | Morphine stimulates CCL2 production by human neurons |
| title_fullStr | Morphine stimulates CCL2 production by human neurons |
| title_full_unstemmed | Morphine stimulates CCL2 production by human neurons |
| title_short | Morphine stimulates CCL2 production by human neurons |
| title_sort | morphine stimulates ccl2 production by human neurons |
| url | http://www.jneuroinflammation.com/content/3/1/32 |
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