The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle?

In a recent study, the difference between asthma and eosinophilic bronchitis (a condition characterized by cough but not airway hyperresponsiveness or airflow obstruction) was infiltration of airway smooth muscle (ASM) by mast cells. Mast cells produce a variety of lipid mediators, chemokines, cytok...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of allergy and clinical immunology 2004-07, Vol.114 (1), p.58-65
1. Verfasser: Robinson, Douglas S
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 65
container_issue 1
container_start_page 58
container_title Journal of allergy and clinical immunology
container_volume 114
creator Robinson, Douglas S
description In a recent study, the difference between asthma and eosinophilic bronchitis (a condition characterized by cough but not airway hyperresponsiveness or airflow obstruction) was infiltration of airway smooth muscle (ASM) by mast cells. Mast cells produce a variety of lipid mediators, chemokines, cytokines, and enzymes that may interact with ASM cells to cause hyperreactivity to constrictive stimuli and proliferation, and activated ASM can produce stem cell factor and other chemokines, cytokines, and growth factors that may act in recruitment, differentiation, and retention of mast cells. Mast cell infiltration of the airways in asthma is T-cell–dependent, and TH2 cytokines from T cells and other sources act in mast cell expansion from circulating and tissue precursors. The recent data on interactions of mast cells and ASM suggest that this could be an important contributor to airway hyperresponsiveness in asthma. Why this occurs in asthma and how it is sustained remain to be established.
doi_str_mv 10.1016/j.jaci.2004.03.034
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_66685328</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0091674904011662</els_id><sourcerecordid>66685328</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-bb569044da2ab7f6f7764696e2c0ddfd8c47c568930c7498da48468f3e5990b23</originalsourceid><addsrcrecordid>eNqFkV9rFDEUxYNY7Lb6BXyQAdG3WfN_EimIlGoLBV_qc8gkd9gMM5M1mWnZb98Mu6D4oHDhnsDvXu7JQegtwVuCifzUb3vrwpZizLeYleIv0IZg3dRSUfESbTDWpJYN1-foIucelzdT-hU6J4JywrjYoPiwgyrFAarYVXPRo81z5WAYqjBVRe9G-7lIv7g5xGmlbEhP9lDtDntICfI-Tjk8wgQ5V-2hoDMke4Sfwryr8hhjaeOS3QBfXqOzzg4Z3pz6Jfr57ebh-ra-__H97vrrfe24EnPdtkJqzLm31LZNJ7umkVxqCdRh7zuvHG-ckEoz7Io_5S1XXKqOgdAat5Rdoo_HvfsUfy2QZzOGvNqyE8QlGymlEoyq_4KkEQxL3BTw_V9gH5c0FROGCMwVU4ryQtEj5VLMOUFn9imMNh0MwWZNzfRmTc2sqRnMSq1D706rl3YE_3vkFFMBPpwAm50dumQnF_IfnGaS69X11ZGD8rWPAZLJLsDkwIcEbjY-hn_d8QwF1rWB</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1504838824</pqid></control><display><type>article</type><title>The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle?</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Robinson, Douglas S</creator><creatorcontrib>Robinson, Douglas S</creatorcontrib><description>In a recent study, the difference between asthma and eosinophilic bronchitis (a condition characterized by cough but not airway hyperresponsiveness or airflow obstruction) was infiltration of airway smooth muscle (ASM) by mast cells. Mast cells produce a variety of lipid mediators, chemokines, cytokines, and enzymes that may interact with ASM cells to cause hyperreactivity to constrictive stimuli and proliferation, and activated ASM can produce stem cell factor and other chemokines, cytokines, and growth factors that may act in recruitment, differentiation, and retention of mast cells. Mast cell infiltration of the airways in asthma is T-cell–dependent, and TH2 cytokines from T cells and other sources act in mast cell expansion from circulating and tissue precursors. The recent data on interactions of mast cells and ASM suggest that this could be an important contributor to airway hyperresponsiveness in asthma. Why this occurs in asthma and how it is sustained remain to be established.</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2004.03.034</identifier><identifier>PMID: 15241345</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>airway smooth muscle ; Allergies ; Animals ; Asthma ; Asthma - immunology ; Asthma - physiopathology ; Biological and medical sciences ; Biology ; Bronchial Hyperreactivity - immunology ; Cell Survival - immunology ; chemokines ; Crystal structure ; Cytokines ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Genotype &amp; phenotype ; Histamine ; Humans ; Hypersensitivity - complications ; Hypersensitivity - immunology ; Immunoglobulin E - immunology ; Immunopathology ; Mast cells ; Mast Cells - immunology ; Mast Cells - physiology ; Medical sciences ; Mice ; Models, Animal ; Muscle, Smooth - immunology ; Phenotype ; Rodents ; Smooth muscle ; Studies</subject><ispartof>Journal of allergy and clinical immunology, 2004-07, Vol.114 (1), p.58-65</ispartof><rights>2004 American Academy of Allergy, Asthma and Immunology</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2004 American Academy of Allergy, Asthma and Immunology</rights><rights>Copyright Elsevier Limited Jul 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-bb569044da2ab7f6f7764696e2c0ddfd8c47c568930c7498da48468f3e5990b23</citedby><cites>FETCH-LOGICAL-c485t-bb569044da2ab7f6f7764696e2c0ddfd8c47c568930c7498da48468f3e5990b23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jaci.2004.03.034$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=15936492$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15241345$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Robinson, Douglas S</creatorcontrib><title>The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle?</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>In a recent study, the difference between asthma and eosinophilic bronchitis (a condition characterized by cough but not airway hyperresponsiveness or airflow obstruction) was infiltration of airway smooth muscle (ASM) by mast cells. Mast cells produce a variety of lipid mediators, chemokines, cytokines, and enzymes that may interact with ASM cells to cause hyperreactivity to constrictive stimuli and proliferation, and activated ASM can produce stem cell factor and other chemokines, cytokines, and growth factors that may act in recruitment, differentiation, and retention of mast cells. Mast cell infiltration of the airways in asthma is T-cell–dependent, and TH2 cytokines from T cells and other sources act in mast cell expansion from circulating and tissue precursors. The recent data on interactions of mast cells and ASM suggest that this could be an important contributor to airway hyperresponsiveness in asthma. Why this occurs in asthma and how it is sustained remain to be established.</description><subject>airway smooth muscle</subject><subject>Allergies</subject><subject>Animals</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Asthma - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Biology</subject><subject>Bronchial Hyperreactivity - immunology</subject><subject>Cell Survival - immunology</subject><subject>chemokines</subject><subject>Crystal structure</subject><subject>Cytokines</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Genotype &amp; phenotype</subject><subject>Histamine</subject><subject>Humans</subject><subject>Hypersensitivity - complications</subject><subject>Hypersensitivity - immunology</subject><subject>Immunoglobulin E - immunology</subject><subject>Immunopathology</subject><subject>Mast cells</subject><subject>Mast Cells - immunology</subject><subject>Mast Cells - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Models, Animal</subject><subject>Muscle, Smooth - immunology</subject><subject>Phenotype</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Studies</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV9rFDEUxYNY7Lb6BXyQAdG3WfN_EimIlGoLBV_qc8gkd9gMM5M1mWnZb98Mu6D4oHDhnsDvXu7JQegtwVuCifzUb3vrwpZizLeYleIv0IZg3dRSUfESbTDWpJYN1-foIucelzdT-hU6J4JywrjYoPiwgyrFAarYVXPRo81z5WAYqjBVRe9G-7lIv7g5xGmlbEhP9lDtDntICfI-Tjk8wgQ5V-2hoDMke4Sfwryr8hhjaeOS3QBfXqOzzg4Z3pz6Jfr57ebh-ra-__H97vrrfe24EnPdtkJqzLm31LZNJ7umkVxqCdRh7zuvHG-ckEoz7Io_5S1XXKqOgdAat5Rdoo_HvfsUfy2QZzOGvNqyE8QlGymlEoyq_4KkEQxL3BTw_V9gH5c0FROGCMwVU4ryQtEj5VLMOUFn9imMNh0MwWZNzfRmTc2sqRnMSq1D706rl3YE_3vkFFMBPpwAm50dumQnF_IfnGaS69X11ZGD8rWPAZLJLsDkwIcEbjY-hn_d8QwF1rWB</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>Robinson, Douglas S</creator><general>Mosby, 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>7X8</scope></search><sort><creationdate>20040701</creationdate><title>The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle?</title><author>Robinson, Douglas S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-bb569044da2ab7f6f7764696e2c0ddfd8c47c568930c7498da48468f3e5990b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>airway smooth muscle</topic><topic>Allergies</topic><topic>Animals</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Asthma - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Biology</topic><topic>Bronchial Hyperreactivity - immunology</topic><topic>Cell Survival - immunology</topic><topic>chemokines</topic><topic>Crystal structure</topic><topic>Cytokines</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Genotype &amp; phenotype</topic><topic>Histamine</topic><topic>Humans</topic><topic>Hypersensitivity - complications</topic><topic>Hypersensitivity - immunology</topic><topic>Immunoglobulin E - immunology</topic><topic>Immunopathology</topic><topic>Mast cells</topic><topic>Mast Cells - immunology</topic><topic>Mast Cells - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Models, Animal</topic><topic>Muscle, Smooth - immunology</topic><topic>Phenotype</topic><topic>Rodents</topic><topic>Smooth muscle</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Robinson, Douglas S</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 &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Robinson, Douglas S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle?</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2004-07-01</date><risdate>2004</risdate><volume>114</volume><issue>1</issue><spage>58</spage><epage>65</epage><pages>58-65</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>In a recent study, the difference between asthma and eosinophilic bronchitis (a condition characterized by cough but not airway hyperresponsiveness or airflow obstruction) was infiltration of airway smooth muscle (ASM) by mast cells. Mast cells produce a variety of lipid mediators, chemokines, cytokines, and enzymes that may interact with ASM cells to cause hyperreactivity to constrictive stimuli and proliferation, and activated ASM can produce stem cell factor and other chemokines, cytokines, and growth factors that may act in recruitment, differentiation, and retention of mast cells. Mast cell infiltration of the airways in asthma is T-cell–dependent, and TH2 cytokines from T cells and other sources act in mast cell expansion from circulating and tissue precursors. The recent data on interactions of mast cells and ASM suggest that this could be an important contributor to airway hyperresponsiveness in asthma. Why this occurs in asthma and how it is sustained remain to be established.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>15241345</pmid><doi>10.1016/j.jaci.2004.03.034</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0091-6749
ispartof Journal of allergy and clinical immunology, 2004-07, Vol.114 (1), p.58-65
issn 0091-6749
1097-6825
language eng
recordid cdi_proquest_miscellaneous_66685328
source MEDLINE; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals
subjects airway smooth muscle
Allergies
Animals
Asthma
Asthma - immunology
Asthma - physiopathology
Biological and medical sciences
Biology
Bronchial Hyperreactivity - immunology
Cell Survival - immunology
chemokines
Crystal structure
Cytokines
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Genotype & phenotype
Histamine
Humans
Hypersensitivity - complications
Hypersensitivity - immunology
Immunoglobulin E - immunology
Immunopathology
Mast cells
Mast Cells - immunology
Mast Cells - physiology
Medical sciences
Mice
Models, Animal
Muscle, Smooth - immunology
Phenotype
Rodents
Smooth muscle
Studies
title The role of the mast cell in asthma: induction of airway hyperresponsiveness by interaction with smooth muscle?
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T22%3A40%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20role%20of%20the%20mast%20cell%20in%20asthma:%20induction%20of%20airway%20hyperresponsiveness%20by%20interaction%20with%20smooth%20muscle?&rft.jtitle=Journal%20of%20allergy%20and%20clinical%20immunology&rft.au=Robinson,%20Douglas%20S&rft.date=2004-07-01&rft.volume=114&rft.issue=1&rft.spage=58&rft.epage=65&rft.pages=58-65&rft.issn=0091-6749&rft.eissn=1097-6825&rft.coden=JACIBY&rft_id=info:doi/10.1016/j.jaci.2004.03.034&rft_dat=%3Cproquest_cross%3E66685328%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1504838824&rft_id=info:pmid/15241345&rft_els_id=S0091674904011662&rfr_iscdi=true