The tachykinin NK1 receptor is crucial for the development of non-atopic airway inflammation and hyperresponsiveness
Mast cell activation, bronchoconstriction, inflammation and airway hyperreactivity are prominent features of non-atopic hypersensitivity reactions in mouse airways. We studied the role of tachykinin receptors in mice that were skin-sensitized with dinitrofluorobenzene (or vehicle) and challenged int...
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| Veröffentlicht in: | European journal of pharmacology 2003-08, Vol.476 (3), p.249-255 |
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| creator | VAN DER KLEIJ, Hanneke P. M KRANEVELD, Aletta D REDEGELD, Frank A. M GERARD, Norma P MORTEAU, Olivier NIJKAMP, Frans P |
| description | Mast cell activation, bronchoconstriction, inflammation and airway hyperreactivity are prominent features of non-atopic hypersensitivity reactions in mouse airways. We studied the role of tachykinin receptors in mice that were skin-sensitized with dinitrofluorobenzene (or vehicle) and challenged intranasally with dinitrobenzene sulfonic acid. Tachykinin NK1 receptor blockade, by treatment with the antagonist RP67580, or absence of the tachykinin NK1 receptor resulted in a strong reduction in the accumulation of neutrophils in the bronchoalveolar lavage fluid, and in the development of tracheal hyperreactivity in mice 48 h after challenge. In contrast, treatment with the tachykinin NK2 receptor antagonist SR48968 did not affect the dinitrofluorobenzene-induced hypersensitivity reaction. We have previously shown that mast cells play a crucial role in the development of non-atopic asthma. However, we did not observe an inhibitory effect of the tachykinin receptor antagonists or the genetic absence of tachykinin NK1 receptors on mast cell protease release. In conclusion, distal from mast cell activation, the tachykinin NK1 receptor is crucial for the infiltration of pulmonary neutrophils and the development of tracheal hyperreactivity in non-atopic asthma. |
| doi_str_mv | 10.1016/s0014-2999(03)02189-7 |
| format | Article |
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M ; KRANEVELD, Aletta D ; REDEGELD, Frank A. M ; GERARD, Norma P ; MORTEAU, Olivier ; NIJKAMP, Frans P</creator><creatorcontrib>VAN DER KLEIJ, Hanneke P. M ; KRANEVELD, Aletta D ; REDEGELD, Frank A. M ; GERARD, Norma P ; MORTEAU, Olivier ; NIJKAMP, Frans P</creatorcontrib><description>Mast cell activation, bronchoconstriction, inflammation and airway hyperreactivity are prominent features of non-atopic hypersensitivity reactions in mouse airways. We studied the role of tachykinin receptors in mice that were skin-sensitized with dinitrofluorobenzene (or vehicle) and challenged intranasally with dinitrobenzene sulfonic acid. Tachykinin NK1 receptor blockade, by treatment with the antagonist RP67580, or absence of the tachykinin NK1 receptor resulted in a strong reduction in the accumulation of neutrophils in the bronchoalveolar lavage fluid, and in the development of tracheal hyperreactivity in mice 48 h after challenge. In contrast, treatment with the tachykinin NK2 receptor antagonist SR48968 did not affect the dinitrofluorobenzene-induced hypersensitivity reaction. We have previously shown that mast cells play a crucial role in the development of non-atopic asthma. However, we did not observe an inhibitory effect of the tachykinin receptor antagonists or the genetic absence of tachykinin NK1 receptors on mast cell protease release. In conclusion, distal from mast cell activation, the tachykinin NK1 receptor is crucial for the infiltration of pulmonary neutrophils and the development of tracheal hyperreactivity in non-atopic asthma.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/s0014-2999(03)02189-7</identifier><identifier>PMID: 12969772</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier</publisher><subject>Administration, Intranasal ; Airway Obstruction - immunology ; Airway Obstruction - metabolism ; Airway Obstruction - physiopathology ; Animals ; Benzamides ; Biological and medical sciences ; Dinitrofluorobenzene - immunology ; Experimental and animal immunopathology. Animal models ; Hypersensitivity - immunology ; Hypersensitivity - metabolism ; Immunopathology ; In Vitro Techniques ; Indoles - pharmacology ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - pathology ; Isoindoles ; Leukocytes - immunology ; Male ; Mast Cells - immunology ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Neurokinin-1 Receptor Antagonists ; Piperidines ; Receptors, Neurokinin-1 - genetics ; Receptors, Neurokinin-1 - metabolism ; Receptors, Neurokinin-2 - antagonists & inhibitors ; Receptors, Neurokinin-2 - metabolism ; Trachea - drug effects ; Trachea - immunology ; Trachea - physiopathology</subject><ispartof>European journal of pharmacology, 2003-08, Vol.476 (3), p.249-255</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-7fe8c0322e801a47b723903b710f5e9880d10731e1643858d44590a1f04a85b73</citedby><cites>FETCH-LOGICAL-c401t-7fe8c0322e801a47b723903b710f5e9880d10731e1643858d44590a1f04a85b73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15098632$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12969772$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VAN DER KLEIJ, Hanneke P. M</creatorcontrib><creatorcontrib>KRANEVELD, Aletta D</creatorcontrib><creatorcontrib>REDEGELD, Frank A. M</creatorcontrib><creatorcontrib>GERARD, Norma P</creatorcontrib><creatorcontrib>MORTEAU, Olivier</creatorcontrib><creatorcontrib>NIJKAMP, Frans P</creatorcontrib><title>The tachykinin NK1 receptor is crucial for the development of non-atopic airway inflammation and hyperresponsiveness</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Mast cell activation, bronchoconstriction, inflammation and airway hyperreactivity are prominent features of non-atopic hypersensitivity reactions in mouse airways. We studied the role of tachykinin receptors in mice that were skin-sensitized with dinitrofluorobenzene (or vehicle) and challenged intranasally with dinitrobenzene sulfonic acid. Tachykinin NK1 receptor blockade, by treatment with the antagonist RP67580, or absence of the tachykinin NK1 receptor resulted in a strong reduction in the accumulation of neutrophils in the bronchoalveolar lavage fluid, and in the development of tracheal hyperreactivity in mice 48 h after challenge. In contrast, treatment with the tachykinin NK2 receptor antagonist SR48968 did not affect the dinitrofluorobenzene-induced hypersensitivity reaction. We have previously shown that mast cells play a crucial role in the development of non-atopic asthma. However, we did not observe an inhibitory effect of the tachykinin receptor antagonists or the genetic absence of tachykinin NK1 receptors on mast cell protease release. In conclusion, distal from mast cell activation, the tachykinin NK1 receptor is crucial for the infiltration of pulmonary neutrophils and the development of tracheal hyperreactivity in non-atopic asthma.</description><subject>Administration, Intranasal</subject><subject>Airway Obstruction - immunology</subject><subject>Airway Obstruction - metabolism</subject><subject>Airway Obstruction - physiopathology</subject><subject>Animals</subject><subject>Benzamides</subject><subject>Biological and medical sciences</subject><subject>Dinitrofluorobenzene - immunology</subject><subject>Experimental and animal immunopathology. Animal models</subject><subject>Hypersensitivity - immunology</subject><subject>Hypersensitivity - metabolism</subject><subject>Immunopathology</subject><subject>In Vitro Techniques</subject><subject>Indoles - pharmacology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Isoindoles</subject><subject>Leukocytes - immunology</subject><subject>Male</subject><subject>Mast Cells - immunology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Neurokinin-1 Receptor Antagonists</subject><subject>Piperidines</subject><subject>Receptors, Neurokinin-1 - genetics</subject><subject>Receptors, Neurokinin-1 - metabolism</subject><subject>Receptors, Neurokinin-2 - antagonists & inhibitors</subject><subject>Receptors, Neurokinin-2 - metabolism</subject><subject>Trachea - drug effects</subject><subject>Trachea - immunology</subject><subject>Trachea - physiopathology</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0EFvFCEUwHFiauy2-hE0XGraw-gDZgY4No1tjY0erGfCMo8sdgamwNbst3fWbuzp5SU_eMmfkPcMPjFg_ecCwNqGa63PQVwAZ0o38hVZMSV1A5LxI7L6T47JSSm_AaDTvHtDjhnXvZaSr0i93yCt1m12DyGGSL9_YzSjw7mmTEOhLm9dsCP1y1oXOuATjmmeMFaaPI0pNramOThqQ_5jdzREP9ppsjWkSG0c6GY3Y85Y5hRLeMKIpbwlr70dC747zFPy6_rL_dVtc_fj5uvV5V3jWmC1kR6VA8E5KmC2lWvJhQaxlgx8h1opGBhIwZD1rVCdGtq202CZh9aqbi3FKfn4_O-c0-MWSzVTKA7H0UZM22Kk6MUSAhbYPUOXUykZvZlzmGzeGQZmn9v83Lc0-5YGhPmX2-wPfDgc2K4nHF5eHfou4OwAbHF29NlGF8qL60CrXnDxF9RGiNo</recordid><startdate>20030829</startdate><enddate>20030829</enddate><creator>VAN DER KLEIJ, Hanneke P. M</creator><creator>KRANEVELD, Aletta D</creator><creator>REDEGELD, Frank A. M</creator><creator>GERARD, Norma P</creator><creator>MORTEAU, Olivier</creator><creator>NIJKAMP, Frans P</creator><general>Elsevier</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>7X8</scope></search><sort><creationdate>20030829</creationdate><title>The tachykinin NK1 receptor is crucial for the development of non-atopic airway inflammation and hyperresponsiveness</title><author>VAN DER KLEIJ, Hanneke P. M ; KRANEVELD, Aletta D ; REDEGELD, Frank A. M ; GERARD, Norma P ; MORTEAU, Olivier ; NIJKAMP, Frans P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-7fe8c0322e801a47b723903b710f5e9880d10731e1643858d44590a1f04a85b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Administration, Intranasal</topic><topic>Airway Obstruction - immunology</topic><topic>Airway Obstruction - metabolism</topic><topic>Airway Obstruction - physiopathology</topic><topic>Animals</topic><topic>Benzamides</topic><topic>Biological and medical sciences</topic><topic>Dinitrofluorobenzene - immunology</topic><topic>Experimental and animal immunopathology. Animal models</topic><topic>Hypersensitivity - immunology</topic><topic>Hypersensitivity - metabolism</topic><topic>Immunopathology</topic><topic>In Vitro Techniques</topic><topic>Indoles - pharmacology</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Isoindoles</topic><topic>Leukocytes - immunology</topic><topic>Male</topic><topic>Mast Cells - immunology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Neurokinin-1 Receptor Antagonists</topic><topic>Piperidines</topic><topic>Receptors, Neurokinin-1 - genetics</topic><topic>Receptors, Neurokinin-1 - metabolism</topic><topic>Receptors, Neurokinin-2 - antagonists & inhibitors</topic><topic>Receptors, Neurokinin-2 - metabolism</topic><topic>Trachea - drug effects</topic><topic>Trachea - immunology</topic><topic>Trachea - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VAN DER KLEIJ, Hanneke P. M</creatorcontrib><creatorcontrib>KRANEVELD, Aletta D</creatorcontrib><creatorcontrib>REDEGELD, Frank A. M</creatorcontrib><creatorcontrib>GERARD, Norma P</creatorcontrib><creatorcontrib>MORTEAU, Olivier</creatorcontrib><creatorcontrib>NIJKAMP, Frans P</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>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VAN DER KLEIJ, Hanneke P. M</au><au>KRANEVELD, Aletta D</au><au>REDEGELD, Frank A. M</au><au>GERARD, Norma P</au><au>MORTEAU, Olivier</au><au>NIJKAMP, Frans P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The tachykinin NK1 receptor is crucial for the development of non-atopic airway inflammation and hyperresponsiveness</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2003-08-29</date><risdate>2003</risdate><volume>476</volume><issue>3</issue><spage>249</spage><epage>255</epage><pages>249-255</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Mast cell activation, bronchoconstriction, inflammation and airway hyperreactivity are prominent features of non-atopic hypersensitivity reactions in mouse airways. We studied the role of tachykinin receptors in mice that were skin-sensitized with dinitrofluorobenzene (or vehicle) and challenged intranasally with dinitrobenzene sulfonic acid. Tachykinin NK1 receptor blockade, by treatment with the antagonist RP67580, or absence of the tachykinin NK1 receptor resulted in a strong reduction in the accumulation of neutrophils in the bronchoalveolar lavage fluid, and in the development of tracheal hyperreactivity in mice 48 h after challenge. In contrast, treatment with the tachykinin NK2 receptor antagonist SR48968 did not affect the dinitrofluorobenzene-induced hypersensitivity reaction. We have previously shown that mast cells play a crucial role in the development of non-atopic asthma. However, we did not observe an inhibitory effect of the tachykinin receptor antagonists or the genetic absence of tachykinin NK1 receptors on mast cell protease release. In conclusion, distal from mast cell activation, the tachykinin NK1 receptor is crucial for the infiltration of pulmonary neutrophils and the development of tracheal hyperreactivity in non-atopic asthma.</abstract><cop>Amsterdam</cop><pub>Elsevier</pub><pmid>12969772</pmid><doi>10.1016/s0014-2999(03)02189-7</doi><tpages>7</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 2003-08, Vol.476 (3), p.249-255 |
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| subjects | Administration, Intranasal Airway Obstruction - immunology Airway Obstruction - metabolism Airway Obstruction - physiopathology Animals Benzamides Biological and medical sciences Dinitrofluorobenzene - immunology Experimental and animal immunopathology. Animal models Hypersensitivity - immunology Hypersensitivity - metabolism Immunopathology In Vitro Techniques Indoles - pharmacology Inflammation - immunology Inflammation - metabolism Inflammation - pathology Isoindoles Leukocytes - immunology Male Mast Cells - immunology Medical sciences Mice Mice, Inbred BALB C Mice, Knockout Neurokinin-1 Receptor Antagonists Piperidines Receptors, Neurokinin-1 - genetics Receptors, Neurokinin-1 - metabolism Receptors, Neurokinin-2 - antagonists & inhibitors Receptors, Neurokinin-2 - metabolism Trachea - drug effects Trachea - immunology Trachea - physiopathology |
| title | The tachykinin NK1 receptor is crucial for the development of non-atopic airway inflammation and hyperresponsiveness |
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