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The phagocytic capacity of neurones
Phagocytosis is defined as the ingestion of particulates over 0.5 µm in diameter and is associated with cells of the immune system such as macrophages or monocytes. Neurones are not generally recognized to be phagocytic. Using light, confocal, time‐lapse and electron microscopy, we carried out a wid...
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| Published in: | The European journal of neuroscience 2007-05, Vol.25 (10), p.2947-2955 |
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| creator | Bowen, Samantha Ateh, Davidson D. Deinhardt, Katrin Bird, Margaret M. Price, Karen M. Baker, Cathy S. Robson, Joanna C. Swash, Michael Shamsuddin, Wassim Kawar, Shalini El-Tawil, Tariq Roos, Jesper Hoyle, Andrew Nickols, Carole D. Knowles, Charles H. Pullen, Anthony H. Luthert, Phillip J. Weller, Roy O. Hafezparast, Majid Franklin, Robin J. M. Revesz, Tamas King, Rosalind H. M. Berninghausen, Otto Fisher, Elizabeth M. C. Schiavo, Giampietro Martin, Joanne E. |
| description | Phagocytosis is defined as the ingestion of particulates over 0.5 µm in diameter and is associated with cells of the immune system such as macrophages or monocytes. Neurones are not generally recognized to be phagocytic. Using light, confocal, time‐lapse and electron microscopy, we carried out a wide range of in‐vitro and in‐vivo experiments to examine the phagocytic capacity of different neuronal cell types. We demonstrated phagocytosis of material by neurones, including cell debris and synthetic particles up to 2.8 µm in diameter. We showed phagocytosis in different neuronal types, and demonstrated that debris can be transported from neurite extremities to cell bodies and persist within neurones. Flow cytometry analysis demonstrated the lack of certain complement receptors on neurones but the presence of others, including integrin receptors known to mediate macrophage phagocytosis, indicating that a restricted set of phagocytosis receptors may mediate this process. Neuronal phagocytosis occurs in vitro and in vivo, and we propose that this is a more widespread and significant process than previously recognized. Neuronal phagocytosis may explain certain inclusions in neurones during disease, cell‐to‐cell spread of disease, neuronal death during disease progression and provide a potential mechanism for therapeutic intervention through the delivery of particulate drug carriers. |
| doi_str_mv | 10.1111/j.1460-9568.2007.05554.x |
| format | article |
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Using light, confocal, time‐lapse and electron microscopy, we carried out a wide range of in‐vitro and in‐vivo experiments to examine the phagocytic capacity of different neuronal cell types. We demonstrated phagocytosis of material by neurones, including cell debris and synthetic particles up to 2.8 µm in diameter. We showed phagocytosis in different neuronal types, and demonstrated that debris can be transported from neurite extremities to cell bodies and persist within neurones. Flow cytometry analysis demonstrated the lack of certain complement receptors on neurones but the presence of others, including integrin receptors known to mediate macrophage phagocytosis, indicating that a restricted set of phagocytosis receptors may mediate this process. Neuronal phagocytosis occurs in vitro and in vivo, and we propose that this is a more widespread and significant process than previously recognized. Neuronal phagocytosis may explain certain inclusions in neurones during disease, cell‐to‐cell spread of disease, neuronal death during disease progression and provide a potential mechanism for therapeutic intervention through the delivery of particulate drug carriers.</description><identifier>ISSN: 0953-816X</identifier><identifier>EISSN: 1460-9568</identifier><identifier>DOI: 10.1111/j.1460-9568.2007.05554.x</identifier><identifier>PMID: 17561810</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Axons - metabolism ; Axons - ultrastructure ; Chick Embryo ; Cytoplasm - metabolism ; Cytoplasm - ultrastructure ; Dendrites - metabolism ; Dendrites - ultrastructure ; Flow Cytometry ; Ganglia, Spinal - metabolism ; Ganglia, Spinal - ultrastructure ; Humans ; inclusion bodies ; Integrins - metabolism ; Mice ; Mice, Inbred BALB C ; Microscopy, Electron ; Motor Neurons - metabolism ; Motor Neurons - ultrastructure ; Nervous System - metabolism ; Nervous System - ultrastructure ; neurodegeneration ; neurone ; Neurons - metabolism ; Neurons - ultrastructure ; phagocytosis ; Phagocytosis - physiology ; Rats ; Rats, Wistar ; Receptors, Cell Surface - metabolism</subject><ispartof>The European journal of neuroscience, 2007-05, Vol.25 (10), p.2947-2955</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5024-3861306ff7b5b56e2c7157c8e48bb1ed31fe5048c8898d8f1428912290d60cf83</citedby><cites>FETCH-LOGICAL-c5024-3861306ff7b5b56e2c7157c8e48bb1ed31fe5048c8898d8f1428912290d60cf83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1460-9568.2007.05554.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1460-9568.2007.05554.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17561810$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bowen, Samantha</creatorcontrib><creatorcontrib>Ateh, Davidson D.</creatorcontrib><creatorcontrib>Deinhardt, Katrin</creatorcontrib><creatorcontrib>Bird, Margaret M.</creatorcontrib><creatorcontrib>Price, Karen M.</creatorcontrib><creatorcontrib>Baker, Cathy S.</creatorcontrib><creatorcontrib>Robson, Joanna C.</creatorcontrib><creatorcontrib>Swash, Michael</creatorcontrib><creatorcontrib>Shamsuddin, Wassim</creatorcontrib><creatorcontrib>Kawar, Shalini</creatorcontrib><creatorcontrib>El-Tawil, Tariq</creatorcontrib><creatorcontrib>Roos, Jesper</creatorcontrib><creatorcontrib>Hoyle, Andrew</creatorcontrib><creatorcontrib>Nickols, Carole D.</creatorcontrib><creatorcontrib>Knowles, Charles H.</creatorcontrib><creatorcontrib>Pullen, Anthony H.</creatorcontrib><creatorcontrib>Luthert, Phillip J.</creatorcontrib><creatorcontrib>Weller, Roy O.</creatorcontrib><creatorcontrib>Hafezparast, Majid</creatorcontrib><creatorcontrib>Franklin, Robin J. M.</creatorcontrib><creatorcontrib>Revesz, Tamas</creatorcontrib><creatorcontrib>King, Rosalind H. M.</creatorcontrib><creatorcontrib>Berninghausen, Otto</creatorcontrib><creatorcontrib>Fisher, Elizabeth M. C.</creatorcontrib><creatorcontrib>Schiavo, Giampietro</creatorcontrib><creatorcontrib>Martin, Joanne E.</creatorcontrib><title>The phagocytic capacity of neurones</title><title>The European journal of neuroscience</title><addtitle>Eur J Neurosci</addtitle><description>Phagocytosis is defined as the ingestion of particulates over 0.5 µm in diameter and is associated with cells of the immune system such as macrophages or monocytes. Neurones are not generally recognized to be phagocytic. Using light, confocal, time‐lapse and electron microscopy, we carried out a wide range of in‐vitro and in‐vivo experiments to examine the phagocytic capacity of different neuronal cell types. We demonstrated phagocytosis of material by neurones, including cell debris and synthetic particles up to 2.8 µm in diameter. We showed phagocytosis in different neuronal types, and demonstrated that debris can be transported from neurite extremities to cell bodies and persist within neurones. Flow cytometry analysis demonstrated the lack of certain complement receptors on neurones but the presence of others, including integrin receptors known to mediate macrophage phagocytosis, indicating that a restricted set of phagocytosis receptors may mediate this process. Neuronal phagocytosis occurs in vitro and in vivo, and we propose that this is a more widespread and significant process than previously recognized. Neuronal phagocytosis may explain certain inclusions in neurones during disease, cell‐to‐cell spread of disease, neuronal death during disease progression and provide a potential mechanism for therapeutic intervention through the delivery of particulate drug carriers.</description><subject>Animals</subject><subject>Axons - metabolism</subject><subject>Axons - ultrastructure</subject><subject>Chick Embryo</subject><subject>Cytoplasm - metabolism</subject><subject>Cytoplasm - ultrastructure</subject><subject>Dendrites - metabolism</subject><subject>Dendrites - ultrastructure</subject><subject>Flow Cytometry</subject><subject>Ganglia, Spinal - metabolism</subject><subject>Ganglia, Spinal - ultrastructure</subject><subject>Humans</subject><subject>inclusion bodies</subject><subject>Integrins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microscopy, Electron</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - ultrastructure</subject><subject>Nervous System - metabolism</subject><subject>Nervous System - ultrastructure</subject><subject>neurodegeneration</subject><subject>neurone</subject><subject>Neurons - metabolism</subject><subject>Neurons - ultrastructure</subject><subject>phagocytosis</subject><subject>Phagocytosis - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Cell Surface - metabolism</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqNkE1PwjAYgBujEUT_glli4m3zbbt-7ODBEEAJQQ8YvDVb18kQ2Fy3yP69myN41F7apM_zNn0QcjB4uFl3aw_7HNyAcekRAOEBY8z39ieof7w4RX0IGHUl5m89dGHtGgAk99k56mHBOJYY-uhmsTJOvgrfM12XqXZ0mIc6LWsnS5ydqYpsZ-wlOkvCjTVXh32AXsejxfDRnT1PnoYPM1czIL5LJccUeJKIiEWMG6IFZkJL48sowiamODEMfKmlDGQsE-wTGWBCAog56ETSAbrt5uZF9lkZW6ptarXZbMKdySqrBHBCZfOnv0ACDAec4gaUHaiLzNrCJCov0m1Y1AqDakuqtWqDqTaYakuqn5Jq36jXhzeqaGviX_GQrgHuO-Ar3Zj634PVaDpvT43vdn5qS7M_-mHxobiggqnlfKJmL3y6XE6pGtNvc2eOjw</recordid><startdate>200705</startdate><enddate>200705</enddate><creator>Bowen, Samantha</creator><creator>Ateh, Davidson D.</creator><creator>Deinhardt, Katrin</creator><creator>Bird, Margaret M.</creator><creator>Price, Karen M.</creator><creator>Baker, Cathy S.</creator><creator>Robson, Joanna C.</creator><creator>Swash, Michael</creator><creator>Shamsuddin, Wassim</creator><creator>Kawar, Shalini</creator><creator>El-Tawil, Tariq</creator><creator>Roos, Jesper</creator><creator>Hoyle, Andrew</creator><creator>Nickols, Carole D.</creator><creator>Knowles, Charles H.</creator><creator>Pullen, Anthony H.</creator><creator>Luthert, Phillip J.</creator><creator>Weller, Roy O.</creator><creator>Hafezparast, Majid</creator><creator>Franklin, Robin J. 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M.</au><au>Revesz, Tamas</au><au>King, Rosalind H. M.</au><au>Berninghausen, Otto</au><au>Fisher, Elizabeth M. C.</au><au>Schiavo, Giampietro</au><au>Martin, Joanne E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The phagocytic capacity of neurones</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2007-05</date><risdate>2007</risdate><volume>25</volume><issue>10</issue><spage>2947</spage><epage>2955</epage><pages>2947-2955</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><notes>ArticleID:EJN5554</notes><notes>istex:37D0C85BD9C2AE10B4957C4F610FB5BD380E3D90</notes><notes>ark:/67375/WNG-LP6JWWJ3-F</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Phagocytosis is defined as the ingestion of particulates over 0.5 µm in diameter and is associated with cells of the immune system such as macrophages or monocytes. Neurones are not generally recognized to be phagocytic. Using light, confocal, time‐lapse and electron microscopy, we carried out a wide range of in‐vitro and in‐vivo experiments to examine the phagocytic capacity of different neuronal cell types. We demonstrated phagocytosis of material by neurones, including cell debris and synthetic particles up to 2.8 µm in diameter. We showed phagocytosis in different neuronal types, and demonstrated that debris can be transported from neurite extremities to cell bodies and persist within neurones. Flow cytometry analysis demonstrated the lack of certain complement receptors on neurones but the presence of others, including integrin receptors known to mediate macrophage phagocytosis, indicating that a restricted set of phagocytosis receptors may mediate this process. Neuronal phagocytosis occurs in vitro and in vivo, and we propose that this is a more widespread and significant process than previously recognized. Neuronal phagocytosis may explain certain inclusions in neurones during disease, cell‐to‐cell spread of disease, neuronal death during disease progression and provide a potential mechanism for therapeutic intervention through the delivery of particulate drug carriers.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17561810</pmid><doi>10.1111/j.1460-9568.2007.05554.x</doi><tpages>9</tpages></addata></record> |
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| identifier | ISSN: 0953-816X |
| ispartof | The European journal of neuroscience, 2007-05, Vol.25 (10), p.2947-2955 |
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| language | eng |
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| source | Wiley-Blackwell Journals |
| subjects | Animals Axons - metabolism Axons - ultrastructure Chick Embryo Cytoplasm - metabolism Cytoplasm - ultrastructure Dendrites - metabolism Dendrites - ultrastructure Flow Cytometry Ganglia, Spinal - metabolism Ganglia, Spinal - ultrastructure Humans inclusion bodies Integrins - metabolism Mice Mice, Inbred BALB C Microscopy, Electron Motor Neurons - metabolism Motor Neurons - ultrastructure Nervous System - metabolism Nervous System - ultrastructure neurodegeneration neurone Neurons - metabolism Neurons - ultrastructure phagocytosis Phagocytosis - physiology Rats Rats, Wistar Receptors, Cell Surface - metabolism |
| title | The phagocytic capacity of neurones |
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