Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis
The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine C...
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| Veröffentlicht in: | BMC neuroscience 2013-02, Vol.14 (1), p.19-19, Article 19 |
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| creator | Vilela, Márcia Carvalho Lima, Graciela Kunrath Rodrigues, David Henrique Lacerda-Queiroz, Norinne Pedroso, Vinicius Sousa Pietra Miranda, Aline Silva Rachid, Milene Alvarenga Kroon, Erna Geessien Campos, Marco Antônio Teixeira, Mauro Martins Sellner, Johann Teixeira, Antonio Lucio |
| description | The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis.
Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice.
These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host. |
| doi_str_mv | 10.1186/1471-2202-14-19 |
| format | Article |
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Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice.
These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host.</description><identifier>ISSN: 1471-2202</identifier><identifier>EISSN: 1471-2202</identifier><identifier>DOI: 10.1186/1471-2202-14-19</identifier><identifier>PMID: 23391218</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Antigens, Ly - metabolism ; Blood-brain barrier ; Brain ; Brain - immunology ; Brain - pathology ; Brain - virology ; Care and treatment ; Cell Adhesion - genetics ; Cell Adhesion - immunology ; Chemokines ; Cloning ; Cytokines ; Cytokines - metabolism ; Disease Models, Animal ; Encephalitis ; Encephalitis, Herpes Simplex - genetics ; Encephalitis, Herpes Simplex - immunology ; Encephalitis, Herpes Simplex - pathology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Gene Expression Regulation - genetics ; Health aspects ; Herpes simplex encephalitis ; Herpes simplex virus 1 ; Immune response ; Immunization ; Immunotherapy ; Leukocytes ; Leukocytes - physiology ; Lymphocytes ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy ; Mortality ; Neutrophil Infiltration - physiology ; Neutrophils ; Patient outcomes ; Physiological aspects ; Proteins ; Receptors, CCR5 - deficiency ; Receptors, CCR5 - genetics ; Recruitment ; Rodents ; Statistical analysis</subject><ispartof>BMC neuroscience, 2013-02, Vol.14 (1), p.19-19, Article 19</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Vilela et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Vilela et al.; licensee BioMed Central Ltd. 2013 Vilela et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c587t-941e93f4cd3c8f9e5a045d0fb2679d939e1fd46a78f3027fc520a68866ae40d33</citedby><cites>FETCH-LOGICAL-c587t-941e93f4cd3c8f9e5a045d0fb2679d939e1fd46a78f3027fc520a68866ae40d33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3618319/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3618319/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23391218$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vilela, Márcia Carvalho</creatorcontrib><creatorcontrib>Lima, Graciela Kunrath</creatorcontrib><creatorcontrib>Rodrigues, David Henrique</creatorcontrib><creatorcontrib>Lacerda-Queiroz, Norinne</creatorcontrib><creatorcontrib>Pedroso, Vinicius Sousa Pietra</creatorcontrib><creatorcontrib>Miranda, Aline Silva</creatorcontrib><creatorcontrib>Rachid, Milene Alvarenga</creatorcontrib><creatorcontrib>Kroon, Erna Geessien</creatorcontrib><creatorcontrib>Campos, Marco Antônio</creatorcontrib><creatorcontrib>Teixeira, Mauro Martins</creatorcontrib><creatorcontrib>Sellner, Johann</creatorcontrib><creatorcontrib>Teixeira, Antonio Lucio</creatorcontrib><title>Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis</title><title>BMC neuroscience</title><addtitle>BMC Neurosci</addtitle><description>The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis.
Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice.
These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antigens, Ly - metabolism</subject><subject>Blood-brain barrier</subject><subject>Brain</subject><subject>Brain - immunology</subject><subject>Brain - pathology</subject><subject>Brain - virology</subject><subject>Care and treatment</subject><subject>Cell Adhesion - genetics</subject><subject>Cell Adhesion - immunology</subject><subject>Chemokines</subject><subject>Cloning</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Encephalitis</subject><subject>Encephalitis, Herpes Simplex - genetics</subject><subject>Encephalitis, Herpes Simplex - immunology</subject><subject>Encephalitis, Herpes Simplex - pathology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation - genetics</subject><subject>Health aspects</subject><subject>Herpes simplex encephalitis</subject><subject>Herpes simplex virus 1</subject><subject>Immune response</subject><subject>Immunization</subject><subject>Immunotherapy</subject><subject>Leukocytes</subject><subject>Leukocytes - physiology</subject><subject>Lymphocytes</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Microscopy</subject><subject>Mortality</subject><subject>Neutrophil Infiltration - physiology</subject><subject>Neutrophils</subject><subject>Patient outcomes</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Receptors, CCR5 - deficiency</subject><subject>Receptors, CCR5 - genetics</subject><subject>Recruitment</subject><subject>Rodents</subject><subject>Statistical analysis</subject><issn>1471-2202</issn><issn>1471-2202</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNks1rFTEUxYMo9kPX7mTAjZtpc_Mxk2yEx0OtUFBE1yEvc9OXMjMZk5lC_3sztj5bcSFZ5HLzu4fLySHkFdAzANWcg2ihZoyyGkQN-gk5PnSePqiPyEnO15RCqwR7To4Y5xoYqGPyZbPLODqsoq-226-yCqNLaDPmasRlTnHah75K6NIS5gHHuQBVxhtMWO0xTTgHV60C0972YQ75BXnmbZ_x5f19Sr5_eP9te1Fffv74abu5rJ1U7VxrAai5F67jTnmN0lIhO-p3rGl1p7lG8J1obKs8p6z1TjJqG6WaxqKgHeen5N2d7rTsBuxcWS3Z3kwpDDbdmmiDefwyhr25ijeGN6A46CLw9l4gxR8L5tkMITvseztiXLIBLpRQknLxHygTWqryIwV98xd6HZc0FidWimstNcAf6sr2aMLoY1nRraJmI7mQLVfQFursH1Q5HQ7BxRF9KP1HA-d3Ay7FnBP6gx1AzZoXsybCrIkolfllwuuHLh743wHhPwHN9rjT</recordid><startdate>20130207</startdate><enddate>20130207</enddate><creator>Vilela, Márcia Carvalho</creator><creator>Lima, Graciela Kunrath</creator><creator>Rodrigues, David Henrique</creator><creator>Lacerda-Queiroz, Norinne</creator><creator>Pedroso, Vinicius Sousa Pietra</creator><creator>Miranda, Aline Silva</creator><creator>Rachid, Milene Alvarenga</creator><creator>Kroon, Erna Geessien</creator><creator>Campos, Marco Antônio</creator><creator>Teixeira, Mauro Martins</creator><creator>Sellner, Johann</creator><creator>Teixeira, Antonio Lucio</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>7U9</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20130207</creationdate><title>Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis</title><author>Vilela, Márcia Carvalho ; Lima, Graciela Kunrath ; Rodrigues, David Henrique ; Lacerda-Queiroz, Norinne ; Pedroso, Vinicius Sousa Pietra ; Miranda, Aline Silva ; Rachid, Milene Alvarenga ; Kroon, Erna Geessien ; Campos, Marco Antônio ; Teixeira, Mauro Martins ; Sellner, Johann ; Teixeira, Antonio Lucio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c587t-941e93f4cd3c8f9e5a045d0fb2679d939e1fd46a78f3027fc520a68866ae40d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antigens, Ly - metabolism</topic><topic>Blood-brain barrier</topic><topic>Brain</topic><topic>Brain - immunology</topic><topic>Brain - pathology</topic><topic>Brain - virology</topic><topic>Care and treatment</topic><topic>Cell Adhesion - genetics</topic><topic>Cell Adhesion - immunology</topic><topic>Chemokines</topic><topic>Cloning</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Encephalitis</topic><topic>Encephalitis, Herpes Simplex - genetics</topic><topic>Encephalitis, Herpes Simplex - immunology</topic><topic>Encephalitis, Herpes Simplex - pathology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Flow Cytometry</topic><topic>Gene Expression Regulation - genetics</topic><topic>Health aspects</topic><topic>Herpes simplex encephalitis</topic><topic>Herpes simplex virus 1</topic><topic>Immune response</topic><topic>Immunization</topic><topic>Immunotherapy</topic><topic>Leukocytes</topic><topic>Leukocytes - physiology</topic><topic>Lymphocytes</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Microscopy</topic><topic>Mortality</topic><topic>Neutrophil Infiltration - physiology</topic><topic>Neutrophils</topic><topic>Patient outcomes</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Receptors, CCR5 - deficiency</topic><topic>Receptors, CCR5 - genetics</topic><topic>Recruitment</topic><topic>Rodents</topic><topic>Statistical analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vilela, Márcia Carvalho</creatorcontrib><creatorcontrib>Lima, Graciela Kunrath</creatorcontrib><creatorcontrib>Rodrigues, David Henrique</creatorcontrib><creatorcontrib>Lacerda-Queiroz, Norinne</creatorcontrib><creatorcontrib>Pedroso, Vinicius Sousa Pietra</creatorcontrib><creatorcontrib>Miranda, Aline Silva</creatorcontrib><creatorcontrib>Rachid, Milene Alvarenga</creatorcontrib><creatorcontrib>Kroon, Erna Geessien</creatorcontrib><creatorcontrib>Campos, Marco Antônio</creatorcontrib><creatorcontrib>Teixeira, Mauro Martins</creatorcontrib><creatorcontrib>Sellner, Johann</creatorcontrib><creatorcontrib>Teixeira, Antonio Lucio</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>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest SciTech 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>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>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vilela, Márcia Carvalho</au><au>Lima, Graciela Kunrath</au><au>Rodrigues, David Henrique</au><au>Lacerda-Queiroz, Norinne</au><au>Pedroso, Vinicius Sousa Pietra</au><au>Miranda, Aline Silva</au><au>Rachid, Milene Alvarenga</au><au>Kroon, Erna Geessien</au><au>Campos, Marco Antônio</au><au>Teixeira, Mauro Martins</au><au>Sellner, Johann</au><au>Teixeira, Antonio Lucio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis</atitle><jtitle>BMC neuroscience</jtitle><addtitle>BMC Neurosci</addtitle><date>2013-02-07</date><risdate>2013</risdate><volume>14</volume><issue>1</issue><spage>19</spage><epage>19</epage><pages>19-19</pages><artnum>19</artnum><issn>1471-2202</issn><eissn>1471-2202</eissn><abstract>The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis.
Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice.
These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23391218</pmid><doi>10.1186/1471-2202-14-19</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Antigens, Ly - metabolism Blood-brain barrier Brain Brain - immunology Brain - pathology Brain - virology Care and treatment Cell Adhesion - genetics Cell Adhesion - immunology Chemokines Cloning Cytokines Cytokines - metabolism Disease Models, Animal Encephalitis Encephalitis, Herpes Simplex - genetics Encephalitis, Herpes Simplex - immunology Encephalitis, Herpes Simplex - pathology Enzyme-Linked Immunosorbent Assay Flow Cytometry Gene Expression Regulation - genetics Health aspects Herpes simplex encephalitis Herpes simplex virus 1 Immune response Immunization Immunotherapy Leukocytes Leukocytes - physiology Lymphocytes Mice Mice, Inbred C57BL Mice, Knockout Microscopy Mortality Neutrophil Infiltration - physiology Neutrophils Patient outcomes Physiological aspects Proteins Receptors, CCR5 - deficiency Receptors, CCR5 - genetics Recruitment Rodents Statistical analysis |
| title | Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis |
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