Modulation of inflammatory pathways by the immune cholinergic system
Research done in the past years pointed to a novel function of cholinergic transmission. It has been shown that cholinergic transmission can modulate various aspects of the immune function, whether innate or adaptive. Cholinergic transmission affects immune cell proliferation, cytokine production, T...
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Veröffentlicht in: | Amino acids 2013-07, Vol.45 (1), p.73-85 |
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description | Research done in the past years pointed to a novel function of cholinergic transmission. It has been shown that cholinergic transmission can modulate various aspects of the immune function, whether innate or adaptive. Cholinergic transmission affects immune cell proliferation, cytokine production, T helper differentiation and antigen presentation. Theses effects are mediated by cholinergic muscarinic and nicotinic receptors and other cholinergic components present in immune cells, such as acetylcholinesterase (AChE) and cholineacetyltransferase. The α7 nicotinic acetylcholine receptor was designated anti-inflammatory activity and has shown promise in pre-clinical models of inflammatory disorders. We herein describe the various components of the immune cholinergic system, and specifically the immune suppressive effects of α7 activation. This activation can be accomplished either by direct stimulation or indirectly, by inhibition of AChE. Thus, the presence of the immune cholinergic system can pave the way for novel immunomodulatory agents, or to the broadening of use of known cholinergic agents. |
doi_str_mv | 10.1007/s00726-011-1192-8 |
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It has been shown that cholinergic transmission can modulate various aspects of the immune function, whether innate or adaptive. Cholinergic transmission affects immune cell proliferation, cytokine production, T helper differentiation and antigen presentation. Theses effects are mediated by cholinergic muscarinic and nicotinic receptors and other cholinergic components present in immune cells, such as acetylcholinesterase (AChE) and cholineacetyltransferase. The α7 nicotinic acetylcholine receptor was designated anti-inflammatory activity and has shown promise in pre-clinical models of inflammatory disorders. We herein describe the various components of the immune cholinergic system, and specifically the immune suppressive effects of α7 activation. This activation can be accomplished either by direct stimulation or indirectly, by inhibition of AChE. Thus, the presence of the immune cholinergic system can pave the way for novel immunomodulatory agents, or to the broadening of use of known cholinergic agents.</description><identifier>ISSN: 0939-4451</identifier><identifier>EISSN: 1438-2199</identifier><identifier>DOI: 10.1007/s00726-011-1192-8</identifier><identifier>PMID: 22194043</identifier><language>eng</language><publisher>Vienna: Springer-Verlag</publisher><subject>Acetylcholine - metabolism ; acetylcholinesterase ; Activation ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Alzheimer Disease - metabolism ; Amino acids ; Analytical Chemistry ; Animals ; anti-inflammatory activity ; antigen presentation ; Antigens ; Biochemical Engineering ; Biochemistry ; Biomedical and Life Sciences ; CD4-positive T-lymphocytes ; Cell Proliferation ; cholinergic agents ; cholinergic receptors ; Cholinergics ; cytokines ; Cytokines - biosynthesis ; Humans ; Inflammation - immunology ; Invited Review ; Life Sciences ; Mathematical models ; Mice ; Modulation ; Multiple Sclerosis - metabolism ; Myasthenia Gravis - metabolism ; Neurobiology ; Neuroimmunomodulation ; Proteomics ; Receptors ; Receptors, Muscarinic - metabolism ; Receptors, Nicotinic - metabolism ; Stimulation ; T-Lymphocytes - immunology</subject><ispartof>Amino acids, 2013-07, Vol.45 (1), p.73-85</ispartof><rights>Springer-Verlag 2011</rights><rights>Springer-Verlag Wien 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-dc7cfc477d34a7714e11a0788d18cc6511be0f1445fbbfd8e07a903158b147703</citedby><cites>FETCH-LOGICAL-c495t-dc7cfc477d34a7714e11a0788d18cc6511be0f1445fbbfd8e07a903158b147703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00726-011-1192-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00726-011-1192-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22194043$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nizri, Eran</creatorcontrib><creatorcontrib>Brenner, Talma</creatorcontrib><title>Modulation of inflammatory pathways by the immune cholinergic system</title><title>Amino acids</title><addtitle>Amino Acids</addtitle><addtitle>Amino Acids</addtitle><description>Research done in the past years pointed to a novel function of cholinergic transmission. It has been shown that cholinergic transmission can modulate various aspects of the immune function, whether innate or adaptive. Cholinergic transmission affects immune cell proliferation, cytokine production, T helper differentiation and antigen presentation. Theses effects are mediated by cholinergic muscarinic and nicotinic receptors and other cholinergic components present in immune cells, such as acetylcholinesterase (AChE) and cholineacetyltransferase. The α7 nicotinic acetylcholine receptor was designated anti-inflammatory activity and has shown promise in pre-clinical models of inflammatory disorders. We herein describe the various components of the immune cholinergic system, and specifically the immune suppressive effects of α7 activation. This activation can be accomplished either by direct stimulation or indirectly, by inhibition of AChE. Thus, the presence of the immune cholinergic system can pave the way for novel immunomodulatory agents, or to the broadening of use of known cholinergic agents.</description><subject>Acetylcholine - metabolism</subject><subject>acetylcholinesterase</subject><subject>Activation</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Alzheimer Disease - metabolism</subject><subject>Amino acids</subject><subject>Analytical Chemistry</subject><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>antigen presentation</subject><subject>Antigens</subject><subject>Biochemical Engineering</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>CD4-positive T-lymphocytes</subject><subject>Cell Proliferation</subject><subject>cholinergic agents</subject><subject>cholinergic receptors</subject><subject>Cholinergics</subject><subject>cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Humans</subject><subject>Inflammation - immunology</subject><subject>Invited Review</subject><subject>Life Sciences</subject><subject>Mathematical models</subject><subject>Mice</subject><subject>Modulation</subject><subject>Multiple Sclerosis - metabolism</subject><subject>Myasthenia Gravis - metabolism</subject><subject>Neurobiology</subject><subject>Neuroimmunomodulation</subject><subject>Proteomics</subject><subject>Receptors</subject><subject>Receptors, Muscarinic - metabolism</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Stimulation</subject><subject>T-Lymphocytes - immunology</subject><issn>0939-4451</issn><issn>1438-2199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkU9PwyAYh4nRuDn9AF60iRcvVd6WFno0828y40F3JpTC1qUtE9qYfntpOo3xoBc48PweePkhdAr4CjCm184vURpigBAgi0K2h6ZAYhZGkGX7aIqzOAsJSWCCjpzbYAwRg_QQTSIPEEziKbp9NkVXibY0TWB0UDa6EnUtWmP7YCva9YfoXZD3QbtWQVnXXaMCuTZV2Si7KmXgeteq-hgdaFE5dbLbZ2h5f_c2fwwXLw9P85tFKEmWtGEhqdSSUFrERFAKRAEITBkrgEmZJgC5whr8g3We64IpTEWGY0hYDj6F4xm6HL1ba9475Vpel06qqhKNMp3jQMDbwJv_R-OUMkopST168QvdmM42fpCB8hikZBDCSElrnLNK860ta2F7DpgPbfCxDe7b4EMbnPnM2c7c5bUqvhNf3--BaAScP2pWyv64-g_r-RjSwnCxsqXjy9cIQ4p9wX6gLP4EVfmcXw</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Nizri, Eran</creator><creator>Brenner, Talma</creator><general>Springer-Verlag</general><general>Springer Vienna</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>20130701</creationdate><title>Modulation of inflammatory pathways by the immune cholinergic system</title><author>Nizri, Eran ; Brenner, Talma</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-dc7cfc477d34a7714e11a0788d18cc6511be0f1445fbbfd8e07a903158b147703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acetylcholine - metabolism</topic><topic>acetylcholinesterase</topic><topic>Activation</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Alzheimer Disease - metabolism</topic><topic>Amino acids</topic><topic>Analytical Chemistry</topic><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>antigen presentation</topic><topic>Antigens</topic><topic>Biochemical Engineering</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>CD4-positive T-lymphocytes</topic><topic>Cell Proliferation</topic><topic>cholinergic agents</topic><topic>cholinergic receptors</topic><topic>Cholinergics</topic><topic>cytokines</topic><topic>Cytokines - biosynthesis</topic><topic>Humans</topic><topic>Inflammation - immunology</topic><topic>Invited Review</topic><topic>Life Sciences</topic><topic>Mathematical models</topic><topic>Mice</topic><topic>Modulation</topic><topic>Multiple Sclerosis - metabolism</topic><topic>Myasthenia Gravis - metabolism</topic><topic>Neurobiology</topic><topic>Neuroimmunomodulation</topic><topic>Proteomics</topic><topic>Receptors</topic><topic>Receptors, Muscarinic - metabolism</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>Stimulation</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nizri, Eran</creatorcontrib><creatorcontrib>Brenner, Talma</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Materials Science Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Amino acids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nizri, Eran</au><au>Brenner, Talma</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of inflammatory pathways by the immune cholinergic system</atitle><jtitle>Amino acids</jtitle><stitle>Amino Acids</stitle><addtitle>Amino Acids</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>45</volume><issue>1</issue><spage>73</spage><epage>85</epage><pages>73-85</pages><issn>0939-4451</issn><eissn>1438-2199</eissn><abstract>Research done in the past years pointed to a novel function of cholinergic transmission. It has been shown that cholinergic transmission can modulate various aspects of the immune function, whether innate or adaptive. Cholinergic transmission affects immune cell proliferation, cytokine production, T helper differentiation and antigen presentation. Theses effects are mediated by cholinergic muscarinic and nicotinic receptors and other cholinergic components present in immune cells, such as acetylcholinesterase (AChE) and cholineacetyltransferase. The α7 nicotinic acetylcholine receptor was designated anti-inflammatory activity and has shown promise in pre-clinical models of inflammatory disorders. We herein describe the various components of the immune cholinergic system, and specifically the immune suppressive effects of α7 activation. This activation can be accomplished either by direct stimulation or indirectly, by inhibition of AChE. Thus, the presence of the immune cholinergic system can pave the way for novel immunomodulatory agents, or to the broadening of use of known cholinergic agents.</abstract><cop>Vienna</cop><pub>Springer-Verlag</pub><pmid>22194043</pmid><doi>10.1007/s00726-011-1192-8</doi><tpages>13</tpages></addata></record> |
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subjects | Acetylcholine - metabolism acetylcholinesterase Activation alpha7 Nicotinic Acetylcholine Receptor - metabolism Alzheimer Disease - metabolism Amino acids Analytical Chemistry Animals anti-inflammatory activity antigen presentation Antigens Biochemical Engineering Biochemistry Biomedical and Life Sciences CD4-positive T-lymphocytes Cell Proliferation cholinergic agents cholinergic receptors Cholinergics cytokines Cytokines - biosynthesis Humans Inflammation - immunology Invited Review Life Sciences Mathematical models Mice Modulation Multiple Sclerosis - metabolism Myasthenia Gravis - metabolism Neurobiology Neuroimmunomodulation Proteomics Receptors Receptors, Muscarinic - metabolism Receptors, Nicotinic - metabolism Stimulation T-Lymphocytes - immunology |
title | Modulation of inflammatory pathways by the immune cholinergic system |
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