Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation
Leukocyte recruitment from blood to inflammatory sites occurs in a multistep process that involves discrete molecular interactions between circulating and endothelial cells. Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral t...
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Veröffentlicht in: | The Journal of immunology (1950) 2005-05, Vol.174 (10), p.6406-6415 |
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container_title | The Journal of immunology (1950) |
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creator | Aurrand-Lions, Michel Lamagna, Chrystelle Dangerfield, John P Wang, Shijun Herrera, Pedro Nourshargh, Sussan Imhof, Beat A |
description | Leukocyte recruitment from blood to inflammatory sites occurs in a multistep process that involves discrete molecular interactions between circulating and endothelial cells. Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral tissues and has been proposed to regulate neutrophil migration by its interaction with the leukocyte integrin Mac-1. In the present study, we show that the accumulation of leukocytes in alveoli during acute pulmonary inflammation in mice is partially blocked using neutralizing Abs against JAM-C. To confirm the function of JAM-C in regulating leukocyte migration in vivo, we then generated a strain of transgenic mice overexpressing JAM-C under the control of the endothelial specific promotor Tie2. The transgenic animals accumulate more leukocytes to inflammatory sites compared with littermate control mice. Intravital microscopy shows that this is the result of increased leukocyte adhesion and transmigration, whereas rolling of leukocytes is not significantly affected in transgenic mice compared with littermates. Thus, JAM-C participates in the later steps of the leukoendothelial adhesion cascade. |
doi_str_mv | 10.4049/jimmunol.174.10.6406 |
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Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral tissues and has been proposed to regulate neutrophil migration by its interaction with the leukocyte integrin Mac-1. In the present study, we show that the accumulation of leukocytes in alveoli during acute pulmonary inflammation in mice is partially blocked using neutralizing Abs against JAM-C. To confirm the function of JAM-C in regulating leukocyte migration in vivo, we then generated a strain of transgenic mice overexpressing JAM-C under the control of the endothelial specific promotor Tie2. The transgenic animals accumulate more leukocytes to inflammatory sites compared with littermate control mice. Intravital microscopy shows that this is the result of increased leukocyte adhesion and transmigration, whereas rolling of leukocytes is not significantly affected in transgenic mice compared with littermates. Thus, JAM-C participates in the later steps of the leukoendothelial adhesion cascade.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.174.10.6406</identifier><identifier>PMID: 15879142</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Acute Disease ; Animals ; Cell Adhesion - genetics ; Cell Adhesion - immunology ; Cell Adhesion Molecules - biosynthesis ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - physiology ; Cell Line, Tumor ; Chemotaxis, Leukocyte - genetics ; Chemotaxis, Leukocyte - immunology ; Endothelium - immunology ; Endothelium - metabolism ; Endothelium - pathology ; Granulocytes - cytology ; Granulocytes - immunology ; Granulocytes - metabolism ; Immunoglobulins - biosynthesis ; Immunoglobulins - genetics ; Immunoglobulins - physiology ; Inflammation Mediators - metabolism ; Inflammation Mediators - physiology ; Lung - immunology ; Lung - pathology ; Membrane Proteins - biosynthesis ; Membrane Proteins - genetics ; Membrane Proteins - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Video ; Monocytes - cytology ; Monocytes - immunology ; Monocytes - metabolism ; Neutrophil Infiltration - genetics ; Neutrophil Infiltration - immunology ; Time Factors</subject><ispartof>The Journal of immunology (1950), 2005-05, Vol.174 (10), p.6406-6415</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-38fc497999220579fe03256558eddc46d00a375d399101b66733c37e595cb4753</citedby><cites>FETCH-LOGICAL-c415t-38fc497999220579fe03256558eddc46d00a375d399101b66733c37e595cb4753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15879142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aurrand-Lions, Michel</creatorcontrib><creatorcontrib>Lamagna, Chrystelle</creatorcontrib><creatorcontrib>Dangerfield, John P</creatorcontrib><creatorcontrib>Wang, Shijun</creatorcontrib><creatorcontrib>Herrera, Pedro</creatorcontrib><creatorcontrib>Nourshargh, Sussan</creatorcontrib><creatorcontrib>Imhof, Beat A</creatorcontrib><title>Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Leukocyte recruitment from blood to inflammatory sites occurs in a multistep process that involves discrete molecular interactions between circulating and endothelial cells. Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral tissues and has been proposed to regulate neutrophil migration by its interaction with the leukocyte integrin Mac-1. In the present study, we show that the accumulation of leukocytes in alveoli during acute pulmonary inflammation in mice is partially blocked using neutralizing Abs against JAM-C. To confirm the function of JAM-C in regulating leukocyte migration in vivo, we then generated a strain of transgenic mice overexpressing JAM-C under the control of the endothelial specific promotor Tie2. The transgenic animals accumulate more leukocytes to inflammatory sites compared with littermate control mice. Intravital microscopy shows that this is the result of increased leukocyte adhesion and transmigration, whereas rolling of leukocytes is not significantly affected in transgenic mice compared with littermates. Thus, JAM-C participates in the later steps of the leukoendothelial adhesion cascade.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Cell Adhesion - genetics</subject><subject>Cell Adhesion - immunology</subject><subject>Cell Adhesion Molecules - biosynthesis</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - physiology</subject><subject>Cell Line, Tumor</subject><subject>Chemotaxis, Leukocyte - genetics</subject><subject>Chemotaxis, Leukocyte - immunology</subject><subject>Endothelium - immunology</subject><subject>Endothelium - metabolism</subject><subject>Endothelium - pathology</subject><subject>Granulocytes - cytology</subject><subject>Granulocytes - immunology</subject><subject>Granulocytes - metabolism</subject><subject>Immunoglobulins - biosynthesis</subject><subject>Immunoglobulins - genetics</subject><subject>Immunoglobulins - physiology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammation Mediators - physiology</subject><subject>Lung - immunology</subject><subject>Lung - pathology</subject><subject>Membrane Proteins - biosynthesis</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microscopy, Video</subject><subject>Monocytes - cytology</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Neutrophil Infiltration - genetics</subject><subject>Neutrophil Infiltration - immunology</subject><subject>Time Factors</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV9P2zAUxa1paO3YvsE0-WnaS8q14z_xI6rKxlSEhNhz5DpO4-LELI5V-u1JaCd448n28e8cXd2D0DcCCwZMXexc26Yu-AWRbDGKgoH4gOaEc8iEAPERzQEozYgUcoY-x7gDAAGUfUIzwgupCKNz1PxJnRlc6LTHl1Vj43jFN8Fbk7zNlvjObpPXg414aCxe6d4f8HVX-_SEQ43XNj0Ec5i-XTcEfO9iTOOjSr3rti-gbls95X9BZ7X20X49nefo79Xqfvk7W9_-ul5erjPDCB-yvKgNU1IpRSlwqWoLOeWC88JWlWGiAtC55FWuFAGyEULmucml5YqbDZM8P0c_jrmPffg3zjKUrYvGeq87G1IshSygoIq-CxJZSJB8AtkRNH2Isbd1-di7VveHkkA5VVH-r2L0sEmcqhht30_5adPa6tV02v0I_DwCjds2e9fbMrba-xEn5X6_f5v1DNh9lLA</recordid><startdate>20050515</startdate><enddate>20050515</enddate><creator>Aurrand-Lions, Michel</creator><creator>Lamagna, Chrystelle</creator><creator>Dangerfield, John P</creator><creator>Wang, Shijun</creator><creator>Herrera, Pedro</creator><creator>Nourshargh, Sussan</creator><creator>Imhof, Beat A</creator><general>Am Assoc Immnol</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20050515</creationdate><title>Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation</title><author>Aurrand-Lions, Michel ; Lamagna, Chrystelle ; Dangerfield, John P ; Wang, Shijun ; Herrera, Pedro ; Nourshargh, Sussan ; Imhof, Beat A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-38fc497999220579fe03256558eddc46d00a375d399101b66733c37e595cb4753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Cell Adhesion - genetics</topic><topic>Cell Adhesion - immunology</topic><topic>Cell Adhesion Molecules - biosynthesis</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Adhesion Molecules - physiology</topic><topic>Cell Line, Tumor</topic><topic>Chemotaxis, Leukocyte - genetics</topic><topic>Chemotaxis, Leukocyte - immunology</topic><topic>Endothelium - immunology</topic><topic>Endothelium - metabolism</topic><topic>Endothelium - pathology</topic><topic>Granulocytes - cytology</topic><topic>Granulocytes - immunology</topic><topic>Granulocytes - metabolism</topic><topic>Immunoglobulins - biosynthesis</topic><topic>Immunoglobulins - genetics</topic><topic>Immunoglobulins - physiology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammation Mediators - physiology</topic><topic>Lung - immunology</topic><topic>Lung - pathology</topic><topic>Membrane Proteins - biosynthesis</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Microscopy, Video</topic><topic>Monocytes - cytology</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Neutrophil Infiltration - genetics</topic><topic>Neutrophil Infiltration - immunology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aurrand-Lions, Michel</creatorcontrib><creatorcontrib>Lamagna, Chrystelle</creatorcontrib><creatorcontrib>Dangerfield, John P</creatorcontrib><creatorcontrib>Wang, Shijun</creatorcontrib><creatorcontrib>Herrera, Pedro</creatorcontrib><creatorcontrib>Nourshargh, Sussan</creatorcontrib><creatorcontrib>Imhof, Beat A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aurrand-Lions, Michel</au><au>Lamagna, Chrystelle</au><au>Dangerfield, John P</au><au>Wang, Shijun</au><au>Herrera, Pedro</au><au>Nourshargh, Sussan</au><au>Imhof, Beat A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2005-05-15</date><risdate>2005</risdate><volume>174</volume><issue>10</issue><spage>6406</spage><epage>6415</epage><pages>6406-6415</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Leukocyte recruitment from blood to inflammatory sites occurs in a multistep process that involves discrete molecular interactions between circulating and endothelial cells. Junctional adhesion molecule (JAM)-C is expressed at different levels on endothelial cells of lymphoid organs and peripheral tissues and has been proposed to regulate neutrophil migration by its interaction with the leukocyte integrin Mac-1. In the present study, we show that the accumulation of leukocytes in alveoli during acute pulmonary inflammation in mice is partially blocked using neutralizing Abs against JAM-C. To confirm the function of JAM-C in regulating leukocyte migration in vivo, we then generated a strain of transgenic mice overexpressing JAM-C under the control of the endothelial specific promotor Tie2. The transgenic animals accumulate more leukocytes to inflammatory sites compared with littermate control mice. Intravital microscopy shows that this is the result of increased leukocyte adhesion and transmigration, whereas rolling of leukocytes is not significantly affected in transgenic mice compared with littermates. 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subjects | Acute Disease Animals Cell Adhesion - genetics Cell Adhesion - immunology Cell Adhesion Molecules - biosynthesis Cell Adhesion Molecules - genetics Cell Adhesion Molecules - physiology Cell Line, Tumor Chemotaxis, Leukocyte - genetics Chemotaxis, Leukocyte - immunology Endothelium - immunology Endothelium - metabolism Endothelium - pathology Granulocytes - cytology Granulocytes - immunology Granulocytes - metabolism Immunoglobulins - biosynthesis Immunoglobulins - genetics Immunoglobulins - physiology Inflammation Mediators - metabolism Inflammation Mediators - physiology Lung - immunology Lung - pathology Membrane Proteins - biosynthesis Membrane Proteins - genetics Membrane Proteins - physiology Mice Mice, Inbred C57BL Mice, Transgenic Microscopy, Video Monocytes - cytology Monocytes - immunology Monocytes - metabolism Neutrophil Infiltration - genetics Neutrophil Infiltration - immunology Time Factors |
title | Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation |
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