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Contact Activation via ICAM-1 Induces Changes in Airway Epithelial Permeability in vitro
The role of ICAM-1 in contact activation of the bronchial epithelial cells is elucidated. Direct contact between epithelial cells and leukocytes is required to change transepithelial electrical resistance (TER) of the epithelium. Migration of human neutrophils across the layers of cultured human air...
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Published in: | Immunological investigations 2007, Vol.36 (1), p.59-72 |
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creator | Choi, Hyon Fleming, Neal W. Serikov, Vladimir B. |
description | The role of ICAM-1 in contact activation of the bronchial epithelial cells is elucidated. Direct contact between epithelial cells and leukocytes is required to change transepithelial electrical resistance (TER) of the epithelium. Migration of human neutrophils across the layers of cultured human airway epithelial cells (Calu-3) or primary cow tracheal epithelial cells was induced by an fMLP gradient. Migrating neutrophils decreased TER and increased permeability to albumin. Monoclonal antibodies to ICAM-1 reduced neutrophil migration, thus reducing the changes in TER and changes in the epithelial permeability to albumin. By confocal microscopy, ERK1/2 was found to be locally activated in the epithelial cells at the sites of migration and cross-linking of ICAM-1. Blockade of ERK1/2 by PD98059 decreased the changes in TER which were induced by ICAM-1 cross-linking. Contact activation of the bronchial epithelial cells, involving ICAM-1 via local activation of ERK1/2, is an important mechanism of alteration of the bronchial epithelial permeability. |
doi_str_mv | 10.1080/08820130600745703 |
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Direct contact between epithelial cells and leukocytes is required to change transepithelial electrical resistance (TER) of the epithelium. Migration of human neutrophils across the layers of cultured human airway epithelial cells (Calu-3) or primary cow tracheal epithelial cells was induced by an fMLP gradient. Migrating neutrophils decreased TER and increased permeability to albumin. Monoclonal antibodies to ICAM-1 reduced neutrophil migration, thus reducing the changes in TER and changes in the epithelial permeability to albumin. By confocal microscopy, ERK1/2 was found to be locally activated in the epithelial cells at the sites of migration and cross-linking of ICAM-1. Blockade of ERK1/2 by PD98059 decreased the changes in TER which were induced by ICAM-1 cross-linking. Contact activation of the bronchial epithelial cells, involving ICAM-1 via local activation of ERK1/2, is an important mechanism of alteration of the bronchial epithelial permeability.</description><identifier>ISSN: 0882-0139</identifier><identifier>EISSN: 1532-4311</identifier><identifier>DOI: 10.1080/08820130600745703</identifier><identifier>PMID: 17190650</identifier><language>eng</language><publisher>England: Informa UK Ltd</publisher><subject>Albumins - metabolism ; Animals ; Antibodies - immunology ; Cattle ; Cell Movement ; Cells, Cultured ; Enzyme Activation ; Epithelial Cells - physiology ; epithelium ; Humans ; ICAM-1 ; Intercellular Adhesion Molecule-1 - immunology ; Intercellular Adhesion Molecule-1 - metabolism ; leukocytes ; Leukocytes - physiology ; Lung - physiology ; migration ; Mitogen-Activated Protein Kinase 3 - metabolism ; Permeability ; Phosphorylation ; Trachea - cytology ; Trachea - physiology ; Tumor Cells, Cultured</subject><ispartof>Immunological investigations, 2007, Vol.36 (1), p.59-72</ispartof><rights>2007 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-ed4a309ad4bd889991b138ad9f69bdc026d5fc10bdeeb87acfa1a9534f1ac5823</citedby><cites>FETCH-LOGICAL-c435t-ed4a309ad4bd889991b138ad9f69bdc026d5fc10bdeeb87acfa1a9534f1ac5823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,4043,27956,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17190650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Choi, Hyon</creatorcontrib><creatorcontrib>Fleming, Neal W.</creatorcontrib><creatorcontrib>Serikov, Vladimir B.</creatorcontrib><title>Contact Activation via ICAM-1 Induces Changes in Airway Epithelial Permeability in vitro</title><title>Immunological investigations</title><addtitle>Immunol Invest</addtitle><description>The role of ICAM-1 in contact activation of the bronchial epithelial cells is elucidated. Direct contact between epithelial cells and leukocytes is required to change transepithelial electrical resistance (TER) of the epithelium. Migration of human neutrophils across the layers of cultured human airway epithelial cells (Calu-3) or primary cow tracheal epithelial cells was induced by an fMLP gradient. Migrating neutrophils decreased TER and increased permeability to albumin. Monoclonal antibodies to ICAM-1 reduced neutrophil migration, thus reducing the changes in TER and changes in the epithelial permeability to albumin. By confocal microscopy, ERK1/2 was found to be locally activated in the epithelial cells at the sites of migration and cross-linking of ICAM-1. Blockade of ERK1/2 by PD98059 decreased the changes in TER which were induced by ICAM-1 cross-linking. Contact activation of the bronchial epithelial cells, involving ICAM-1 via local activation of ERK1/2, is an important mechanism of alteration of the bronchial epithelial permeability.</description><subject>Albumins - metabolism</subject><subject>Animals</subject><subject>Antibodies - immunology</subject><subject>Cattle</subject><subject>Cell Movement</subject><subject>Cells, Cultured</subject><subject>Enzyme Activation</subject><subject>Epithelial Cells - physiology</subject><subject>epithelium</subject><subject>Humans</subject><subject>ICAM-1</subject><subject>Intercellular Adhesion Molecule-1 - immunology</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>leukocytes</subject><subject>Leukocytes - physiology</subject><subject>Lung - physiology</subject><subject>migration</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Permeability</subject><subject>Phosphorylation</subject><subject>Trachea - cytology</subject><subject>Trachea - physiology</subject><subject>Tumor Cells, Cultured</subject><issn>0882-0139</issn><issn>1532-4311</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqFkMFuEzEQhi0EoqHwAFzQnrgtHcfrXVtwiaIClVq1B5C4WbO2l7jy2sH2psrbs1EiIVSpPc1hvv-b0U_IewqfKAi4ACGWQBm0AF3DO2AvyIJytqwbRulLsjjs6xmQZ-RNzvcAwHgrX5Mz2lEJLYcF-bWOoaAu1UoXt8PiYqh2Dqur9eqmptVVMJO2uVpvMPyepwvVyqUH3FeXW1c21jv01Z1No8XeeVf2B2LnSopvyasBfbbvTvOc_Px6-WP9vb6-_TbLr2vdMF5qaxpkINE0vRFCSkl7ygQaObSyNxqWreGDptAba3vRoR6QouSsGShqLpbsnHw8ercp_plsLmp0WVvvMdg4ZdUK1nEG_FmQSj6f7-gM0iOoU8w52UFtkxsx7RUFdehdPep9znw4yad-tOZf4lT0DHw5Ai4MMY34EJM3quDexzQkDNplxZ7yf_4vvrHoy0Zjsuo-TinMDT_x3V97jaJ0</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>Choi, Hyon</creator><creator>Fleming, Neal W.</creator><creator>Serikov, Vladimir B.</creator><general>Informa UK Ltd</general><general>Taylor & Francis</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>2007</creationdate><title>Contact Activation via ICAM-1 Induces Changes in Airway Epithelial Permeability in vitro</title><author>Choi, Hyon ; Fleming, Neal W. ; Serikov, Vladimir B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-ed4a309ad4bd889991b138ad9f69bdc026d5fc10bdeeb87acfa1a9534f1ac5823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Albumins - metabolism</topic><topic>Animals</topic><topic>Antibodies - immunology</topic><topic>Cattle</topic><topic>Cell Movement</topic><topic>Cells, Cultured</topic><topic>Enzyme Activation</topic><topic>Epithelial Cells - physiology</topic><topic>epithelium</topic><topic>Humans</topic><topic>ICAM-1</topic><topic>Intercellular Adhesion Molecule-1 - immunology</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>leukocytes</topic><topic>Leukocytes - physiology</topic><topic>Lung - physiology</topic><topic>migration</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Permeability</topic><topic>Phosphorylation</topic><topic>Trachea - cytology</topic><topic>Trachea - physiology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Hyon</creatorcontrib><creatorcontrib>Fleming, Neal W.</creatorcontrib><creatorcontrib>Serikov, Vladimir B.</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>Immunological investigations</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Hyon</au><au>Fleming, Neal W.</au><au>Serikov, Vladimir B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contact Activation via ICAM-1 Induces Changes in Airway Epithelial Permeability in vitro</atitle><jtitle>Immunological investigations</jtitle><addtitle>Immunol Invest</addtitle><date>2007</date><risdate>2007</risdate><volume>36</volume><issue>1</issue><spage>59</spage><epage>72</epage><pages>59-72</pages><issn>0882-0139</issn><eissn>1532-4311</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The role of ICAM-1 in contact activation of the bronchial epithelial cells is elucidated. Direct contact between epithelial cells and leukocytes is required to change transepithelial electrical resistance (TER) of the epithelium. Migration of human neutrophils across the layers of cultured human airway epithelial cells (Calu-3) or primary cow tracheal epithelial cells was induced by an fMLP gradient. Migrating neutrophils decreased TER and increased permeability to albumin. Monoclonal antibodies to ICAM-1 reduced neutrophil migration, thus reducing the changes in TER and changes in the epithelial permeability to albumin. By confocal microscopy, ERK1/2 was found to be locally activated in the epithelial cells at the sites of migration and cross-linking of ICAM-1. Blockade of ERK1/2 by PD98059 decreased the changes in TER which were induced by ICAM-1 cross-linking. Contact activation of the bronchial epithelial cells, involving ICAM-1 via local activation of ERK1/2, is an important mechanism of alteration of the bronchial epithelial permeability.</abstract><cop>England</cop><pub>Informa UK Ltd</pub><pmid>17190650</pmid><doi>10.1080/08820130600745703</doi><tpages>14</tpages></addata></record> |
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subjects | Albumins - metabolism Animals Antibodies - immunology Cattle Cell Movement Cells, Cultured Enzyme Activation Epithelial Cells - physiology epithelium Humans ICAM-1 Intercellular Adhesion Molecule-1 - immunology Intercellular Adhesion Molecule-1 - metabolism leukocytes Leukocytes - physiology Lung - physiology migration Mitogen-Activated Protein Kinase 3 - metabolism Permeability Phosphorylation Trachea - cytology Trachea - physiology Tumor Cells, Cultured |
title | Contact Activation via ICAM-1 Induces Changes in Airway Epithelial Permeability in vitro |
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