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A Transient Decrease in Spleen Size Following Stroke Corresponds to Splenocyte Release into Systemic Circulation
The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examine...
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Published in: | Journal of neuroimmune pharmacology 2012-12, Vol.7 (4), p.1017-1024 |
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description | The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration. |
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Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.</description><identifier>ISSN: 1557-1890</identifier><identifier>EISSN: 1557-1904</identifier><identifier>DOI: 10.1007/s11481-012-9406-8</identifier><identifier>PMID: 23054371</identifier><language>eng</language><publisher>Boston: Birkhäuser-Verlag</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Count ; Cell Movement ; Fluoresceins ; Fluorescent Dyes ; Immunohistochemistry ; Immunology ; Infarction, Middle Cerebral Artery - pathology ; Killer Cells, Natural - physiology ; Laser-Doppler Flowmetry ; Male ; Neurodegeneration ; Neurosciences ; Perspective ; Pharmacology/Toxicology ; Rats ; Rats, Sprague-Dawley ; Rodents ; Spleen - cytology ; Spleen - pathology ; Stroke - blood ; Stroke - pathology ; Succinimides ; Virology</subject><ispartof>Journal of neuroimmune pharmacology, 2012-12, Vol.7 (4), p.1017-1024</ispartof><rights>Springer Science+Business Media New York 2012</rights><rights>Copyright Springer Nature B.V. Dec 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-cdb04a5b3d203f93019d3439d5517de58f2d4f89e36f4df5f3c29ca9ecf5a7a73</citedby><cites>FETCH-LOGICAL-c470t-cdb04a5b3d203f93019d3439d5517de58f2d4f89e36f4df5f3c29ca9ecf5a7a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23054371$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seifert, Hilary A.</creatorcontrib><creatorcontrib>Hall, Aaron A.</creatorcontrib><creatorcontrib>Chapman, Cortney B.</creatorcontrib><creatorcontrib>Collier, Lisa A.</creatorcontrib><creatorcontrib>Willing, Alison E.</creatorcontrib><creatorcontrib>Pennypacker, Keith R.</creatorcontrib><title>A Transient Decrease in Spleen Size Following Stroke Corresponds to Splenocyte Release into Systemic Circulation</title><title>Journal of neuroimmune pharmacology</title><addtitle>J Neuroimmune Pharmacol</addtitle><addtitle>J Neuroimmune Pharmacol</addtitle><description>The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Count</subject><subject>Cell Movement</subject><subject>Fluoresceins</subject><subject>Fluorescent Dyes</subject><subject>Immunohistochemistry</subject><subject>Immunology</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Killer Cells, Natural - physiology</subject><subject>Laser-Doppler Flowmetry</subject><subject>Male</subject><subject>Neurodegeneration</subject><subject>Neurosciences</subject><subject>Perspective</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Spleen - cytology</subject><subject>Spleen - pathology</subject><subject>Stroke - blood</subject><subject>Stroke - pathology</subject><subject>Succinimides</subject><subject>Virology</subject><issn>1557-1890</issn><issn>1557-1904</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp1kUFv1DAQhS1ERUvhB3BBlrhwCZ2J7Tq-IFULhUqVKtFytrzOZHHJ2sFOipZfT5bdVgWJ04xmvnn202PsFcI7BNAnBVE2WAHWlZFwWjVP2BEqpSs0IJ_e942BQ_a8lFsAKSXAM3ZYC1BSaDxiwxm_yS6WQHHkH8hncoV4iPx66InmEn4RP099n36GuOLXY07fiS9SzlSGFNvCx_SHjclvRuJfqN8rbOebMtI6eL4I2U-9G0OKL9hB5_pCL_f1mH09_3iz-FxdXn26WJxdVl5qGCvfLkE6tRRtDaIzAtC0QgrTKoW6JdV0dSu7xpA47WTbqU742nhnyHfKaafFMXu_0x2m5ZpaP_vLrrdDDmuXNza5YP_exPDNrtKdFQobpbcCb_cCOf2YqIx2HYqnvneR0lQs1kIrMCjEjL75B71NU46zPYtGgTYKa5wp3FE-p1IydQ-fQbDbPO0uTzvnabd52ma-ef3YxcPFfYAzUO-AMq_iivKjp_-r-htasa1N</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Seifert, Hilary A.</creator><creator>Hall, Aaron A.</creator><creator>Chapman, Cortney B.</creator><creator>Collier, Lisa A.</creator><creator>Willing, Alison E.</creator><creator>Pennypacker, Keith R.</creator><general>Birkhäuser-Verlag</general><general>Springer Nature B.V</general><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20121201</creationdate><title>A Transient Decrease in Spleen Size Following Stroke Corresponds to Splenocyte Release into Systemic Circulation</title><author>Seifert, Hilary A. ; Hall, Aaron A. ; Chapman, Cortney B. ; Collier, Lisa A. ; Willing, Alison E. ; Pennypacker, Keith R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-cdb04a5b3d203f93019d3439d5517de58f2d4f89e36f4df5f3c29ca9ecf5a7a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Count</topic><topic>Cell Movement</topic><topic>Fluoresceins</topic><topic>Fluorescent Dyes</topic><topic>Immunohistochemistry</topic><topic>Immunology</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Killer Cells, Natural - physiology</topic><topic>Laser-Doppler Flowmetry</topic><topic>Male</topic><topic>Neurodegeneration</topic><topic>Neurosciences</topic><topic>Perspective</topic><topic>Pharmacology/Toxicology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Spleen - cytology</topic><topic>Spleen - pathology</topic><topic>Stroke - blood</topic><topic>Stroke - pathology</topic><topic>Succinimides</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seifert, Hilary A.</creatorcontrib><creatorcontrib>Hall, Aaron A.</creatorcontrib><creatorcontrib>Chapman, Cortney B.</creatorcontrib><creatorcontrib>Collier, Lisa A.</creatorcontrib><creatorcontrib>Willing, Alison E.</creatorcontrib><creatorcontrib>Pennypacker, Keith R.</creatorcontrib><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>Proquest Health & Medical Complete</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuroimmune pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seifert, Hilary A.</au><au>Hall, Aaron A.</au><au>Chapman, Cortney B.</au><au>Collier, Lisa A.</au><au>Willing, Alison E.</au><au>Pennypacker, Keith R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Transient Decrease in Spleen Size Following Stroke Corresponds to Splenocyte Release into Systemic Circulation</atitle><jtitle>Journal of neuroimmune pharmacology</jtitle><stitle>J Neuroimmune Pharmacol</stitle><addtitle>J Neuroimmune Pharmacol</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>7</volume><issue>4</issue><spage>1017</spage><epage>1024</epage><pages>1017-1024</pages><issn>1557-1890</issn><eissn>1557-1904</eissn><abstract>The splenic response to stroke is a proinflammatory reaction to ischemic injury resulting in expanded neurodegeneration. Splenectomy reduces neural injury in rodent models of hemorrhagic and ischemic stroke, however the exact nature of this response has yet to be fully understood. This study examines the migration of splenocytes after brain ischemia utilizing carboxyfluorescein diacetate succinimidyl ester (CFSE) to label them in vivo. The spleen was found to significantly decrease in size from 24 to 48 h following middle cerebral artery occlusion (MCAO) in rats compared to sham operated controls. By 96 h post-MCAO the spleen size returned to levels not different from sham operated rats. To track splenocyte migration following MCAO, spleens were injected with CFSE to label cells. CFSE positive cell numbers were significantly reduced in the 48 h MCAO group versus 48 h sham and CFSE labeled cells were equivalent in 96 h MCAO and sham groups. A significant increase of labeled lymphocyte, monocytes, and neutrophils was detected in the blood at 48 h post-MCAO when compared to the other groups. CFSE labeled cells migrated to the brain following MCAO but appear to remain within the vasculature. These cells were identified as natural killer cells (NK) and monocytes at 48 h and at 96 h post-MCAO NK cells, T cells and monocytes. After ischemic injury, splenocytes enter into systemic circulation and migrate to the brain exacerbating neurodegeneration.</abstract><cop>Boston</cop><pub>Birkhäuser-Verlag</pub><pmid>23054371</pmid><doi>10.1007/s11481-012-9406-8</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biomedical and Life Sciences Biomedicine Cell Biology Cell Count Cell Movement Fluoresceins Fluorescent Dyes Immunohistochemistry Immunology Infarction, Middle Cerebral Artery - pathology Killer Cells, Natural - physiology Laser-Doppler Flowmetry Male Neurodegeneration Neurosciences Perspective Pharmacology/Toxicology Rats Rats, Sprague-Dawley Rodents Spleen - cytology Spleen - pathology Stroke - blood Stroke - pathology Succinimides Virology |
title | A Transient Decrease in Spleen Size Following Stroke Corresponds to Splenocyte Release into Systemic Circulation |
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