Host immune responses to rhinovirus: Mechanisms in asthma
Viral respiratory infections can have a profound effect on many aspects of asthma including its inception, exacerbations, and, possibly, severity. Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated wi...
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Veröffentlicht in: | Journal of allergy and clinical immunology 2008-10, Vol.122 (4), p.671-682 |
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description | Viral respiratory infections can have a profound effect on many aspects of asthma including its inception, exacerbations, and, possibly, severity. Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated with exacerbations and other aspects of asthma. The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many airway cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial cells and possibly macrophages. Infection of epithelial cells generates a variety of proinflammatory mediators to attract inflammatory cells to the airway with a subsequent worsening of underlying disease. Furthermore, there is evidence that the epithelial airway antiviral response to rhinovirus may be defective in asthma. Therefore, understanding the immune response to rhinovirus is a key step in defining mechanisms of asthma, exacerbations, and, perhaps most importantly, improved treatment. |
doi_str_mv | 10.1016/j.jaci.2008.08.013 |
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Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated with exacerbations and other aspects of asthma. The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many airway cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial cells and possibly macrophages. Infection of epithelial cells generates a variety of proinflammatory mediators to attract inflammatory cells to the airway with a subsequent worsening of underlying disease. Furthermore, there is evidence that the epithelial airway antiviral response to rhinovirus may be defective in asthma. Therefore, understanding the immune response to rhinovirus is a key step in defining mechanisms of asthma, exacerbations, and, perhaps most importantly, improved treatment.</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2008.08.013</identifier><identifier>PMID: 19014757</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Accreditation ; Allergies ; Allergy and Immunology ; Asthma ; Asthma - immunology ; Asthma - therapy ; Asthma - virology ; Binding sites ; Biological and medical sciences ; Cell Movement - immunology ; Deoxyribonucleic acid ; DNA ; Drug therapy ; Epithelial Cells - immunology ; Epithelial Cells - virology ; exacerbation ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; immune response to virus ; Immune system ; Immunity, Cellular ; Infections ; Inflammation Mediators - immunology ; Macrophages - immunology ; Macrophages - virology ; Medical sciences ; pathogenesis ; Phylogenetics ; Picornaviridae Infections - immunology ; Picornaviridae Infections - therapy ; Recruitment ; Respiratory Tract Infections - immunology ; Respiratory Tract Infections - therapy ; Respiratory Tract Infections - virology ; Rhinovirus ; Rhinovirus - immunology ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Signal transduction ; Transcription factors ; Viral infections ; Viruses</subject><ispartof>Journal of allergy and clinical immunology, 2008-10, Vol.122 (4), p.671-682</ispartof><rights>American Academy of Allergy, Asthma & Immunology</rights><rights>2008 American Academy of Allergy, Asthma & Immunology</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Elsevier Limited Oct 2008</rights><rights>2008 American Academy of Allergy, Asthma & Immunology 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c597t-2de8859876a8a1a6be9dff97099e43d2f585337232290786daca018ecf42ddd73</citedby><cites>FETCH-LOGICAL-c597t-2de8859876a8a1a6be9dff97099e43d2f585337232290786daca018ecf42ddd73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091674908015066$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20751433$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19014757$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kelly, John T., MD</creatorcontrib><creatorcontrib>Busse, William W., MD</creatorcontrib><title>Host immune responses to rhinovirus: Mechanisms in asthma</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Viral respiratory infections can have a profound effect on many aspects of asthma including its inception, exacerbations, and, possibly, severity. Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated with exacerbations and other aspects of asthma. The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many airway cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial cells and possibly macrophages. Infection of epithelial cells generates a variety of proinflammatory mediators to attract inflammatory cells to the airway with a subsequent worsening of underlying disease. Furthermore, there is evidence that the epithelial airway antiviral response to rhinovirus may be defective in asthma. Therefore, understanding the immune response to rhinovirus is a key step in defining mechanisms of asthma, exacerbations, and, perhaps most importantly, improved treatment.</description><subject>Accreditation</subject><subject>Allergies</subject><subject>Allergy and Immunology</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Asthma - therapy</subject><subject>Asthma - virology</subject><subject>Binding sites</subject><subject>Biological and medical sciences</subject><subject>Cell Movement - immunology</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Drug therapy</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - virology</subject><subject>exacerbation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Humans</subject><subject>immune response to virus</subject><subject>Immune system</subject><subject>Immunity, Cellular</subject><subject>Infections</subject><subject>Inflammation Mediators - immunology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - virology</subject><subject>Medical sciences</subject><subject>pathogenesis</subject><subject>Phylogenetics</subject><subject>Picornaviridae Infections - immunology</subject><subject>Picornaviridae Infections - therapy</subject><subject>Recruitment</subject><subject>Respiratory Tract Infections - immunology</subject><subject>Respiratory Tract Infections - therapy</subject><subject>Respiratory Tract Infections - virology</subject><subject>Rhinovirus</subject><subject>Rhinovirus - immunology</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Signal transduction</subject><subject>Transcription factors</subject><subject>Viral infections</subject><subject>Viruses</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkt9rFDEQxxdR7Fn9B3yQBdG3PfNjs0lEClLUChUf1OeQJrNezt3kmtk96H_vhjta7YPCQAj5zMx38p2qek7JmhLavdmut9aFNSNErUtQ_qBaUaJl0ykmHlYrQjRtOtnqk-oJ4pYsd6704-qEakJbKeSq0hcJpzqM4xyhzoC7FBGwnlKdNyGmfcgzvq2_gNvYGHDEOsTa4rQZ7dPqUW8HhGfH87T68fHD9_OL5vLrp8_n7y8bJ7ScGuZBKaGV7Kyy1HZXoH3fa0m0hpZ71gslOJeMM6aJVJ23zhKqwPUt895LflqdHeru5qsRvIM4ZTuYXQ6jzTcm2WD-folhY36mveGaSd22S4HXxwI5Xc-AkxkDOhgGGyHNaDottSaLiP-BVAuxKFUL-PIeuE1zjssvGCpaqRaElb7sQLmcEDP0t5opMcVAszXFQFMMNCVo0fDiz2nvUo6OLcCrI2DR2aHPNrqAtxwjUtCWl0LvDhws3uwDZIMuQHTgQwY3GZ_Cv3Wc3Ut3Q4hh6fgLbgDv5jXIDDHfyqqVTSOKUEG6jv8GV2LNog</recordid><startdate>20081001</startdate><enddate>20081001</enddate><creator>Kelly, John T., MD</creator><creator>Busse, William W., MD</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</scope><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>7SS</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7U9</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20081001</creationdate><title>Host immune responses to rhinovirus: Mechanisms in asthma</title><author>Kelly, John T., MD ; Busse, William W., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c597t-2de8859876a8a1a6be9dff97099e43d2f585337232290786daca018ecf42ddd73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Accreditation</topic><topic>Allergies</topic><topic>Allergy and Immunology</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Asthma - therapy</topic><topic>Asthma - virology</topic><topic>Binding sites</topic><topic>Biological and medical sciences</topic><topic>Cell Movement - immunology</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Drug therapy</topic><topic>Epithelial Cells - immunology</topic><topic>Epithelial Cells - virology</topic><topic>exacerbation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Humans</topic><topic>immune response to virus</topic><topic>Immune system</topic><topic>Immunity, Cellular</topic><topic>Infections</topic><topic>Inflammation Mediators - immunology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - virology</topic><topic>Medical sciences</topic><topic>pathogenesis</topic><topic>Phylogenetics</topic><topic>Picornaviridae Infections - immunology</topic><topic>Picornaviridae Infections - therapy</topic><topic>Recruitment</topic><topic>Respiratory Tract Infections - immunology</topic><topic>Respiratory Tract Infections - therapy</topic><topic>Respiratory Tract Infections - virology</topic><topic>Rhinovirus</topic><topic>Rhinovirus - immunology</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Signal transduction</topic><topic>Transcription factors</topic><topic>Viral infections</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kelly, John T., MD</creatorcontrib><creatorcontrib>Busse, William W., MD</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Virology and AIDS Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kelly, John T., MD</au><au>Busse, William W., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Host immune responses to rhinovirus: Mechanisms in asthma</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2008-10-01</date><risdate>2008</risdate><volume>122</volume><issue>4</issue><spage>671</spage><epage>682</epage><pages>671-682</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Viral respiratory infections can have a profound effect on many aspects of asthma including its inception, exacerbations, and, possibly, severity. Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated with exacerbations and other aspects of asthma. The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many airway cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial cells and possibly macrophages. Infection of epithelial cells generates a variety of proinflammatory mediators to attract inflammatory cells to the airway with a subsequent worsening of underlying disease. Furthermore, there is evidence that the epithelial airway antiviral response to rhinovirus may be defective in asthma. Therefore, understanding the immune response to rhinovirus is a key step in defining mechanisms of asthma, exacerbations, and, perhaps most importantly, improved treatment.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>19014757</pmid><doi>10.1016/j.jaci.2008.08.013</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Accreditation Allergies Allergy and Immunology Asthma Asthma - immunology Asthma - therapy Asthma - virology Binding sites Biological and medical sciences Cell Movement - immunology Deoxyribonucleic acid DNA Drug therapy Epithelial Cells - immunology Epithelial Cells - virology exacerbation Fundamental and applied biological sciences. Psychology Fundamental immunology Humans immune response to virus Immune system Immunity, Cellular Infections Inflammation Mediators - immunology Macrophages - immunology Macrophages - virology Medical sciences pathogenesis Phylogenetics Picornaviridae Infections - immunology Picornaviridae Infections - therapy Recruitment Respiratory Tract Infections - immunology Respiratory Tract Infections - therapy Respiratory Tract Infections - virology Rhinovirus Rhinovirus - immunology Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Signal transduction Transcription factors Viral infections Viruses |
title | Host immune responses to rhinovirus: Mechanisms in asthma |
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