iNOS depletion completely diminishes reactive nitrogen-species formation after an allergic response
Nitric oxide (NO) shows proinflammatory actions mainly via reactive nitrogen species (RNS) formation through superoxide- and peroxidase-dependent mechanisms. The purpose of this study was to examine the role of inducible NO synthase (iNOS) in RNS production, airway hyperresponsiveness, and inflammat...
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| Veröffentlicht in: | The European respiratory journal 2002-09, Vol.20 (3), p.609-616 |
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| creator | Koarai, A Ichinose, M Sugiura, H Tomaki, M Watanabe, M Yamagata, S Komaki, Y Shirato, K Hattori, T |
| description | Nitric oxide (NO) shows proinflammatory actions mainly via reactive nitrogen species (RNS) formation through superoxide- and peroxidase-dependent mechanisms. The purpose of this study was to examine the role of inducible NO synthase (iNOS) in RNS production, airway hyperresponsiveness, and inflammation after allergen challenge. Ovalbumin (OVA)-sensitised, iNOS-deficient and wild-type mice were used. RNS production was assessed by nitrotyrosine (NT) immunoreactivity in the airways. Airway inflammation and responsiveness were evaluated by eosinophil accumulation and methacholine (i.v.) challenge, respectively. In wild-type mice, OVA-inhalation challenge increased iNOS immunoreactivity in airway epithelial cells as well as iNOS protein measured by Western blotting. The total amounts of nitrite and nitrate in bronchoalveolar lavage (BAL) fluid were increased, and NT immunoreactivity was also observed abundantly in airway inflammatory cells. In iNOS-deficient mice, both iNOS expression and NT formation were completely abolished, and the total amounts of nitrite and nitrate in BAL fluid were significantly decreased. In contrast, OVA-induced airway eosinophil recruitment and hyperresponsiveness were observed almost equally in wild-type and iNOS-deficient mice. These data suggest that reactive nitrogen species production after allergic reaction occurs totally via inducible nitric oxide synthase-dependent pathways. Allergen-mediated airway eosinophil recruitment and hyperresponsiveness appear to be independent of reactive nitrogen species production. |
| doi_str_mv | 10.1183/09031936.02.00274902 |
| format | Article |
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The purpose of this study was to examine the role of inducible NO synthase (iNOS) in RNS production, airway hyperresponsiveness, and inflammation after allergen challenge. Ovalbumin (OVA)-sensitised, iNOS-deficient and wild-type mice were used. RNS production was assessed by nitrotyrosine (NT) immunoreactivity in the airways. Airway inflammation and responsiveness were evaluated by eosinophil accumulation and methacholine (i.v.) challenge, respectively. In wild-type mice, OVA-inhalation challenge increased iNOS immunoreactivity in airway epithelial cells as well as iNOS protein measured by Western blotting. The total amounts of nitrite and nitrate in bronchoalveolar lavage (BAL) fluid were increased, and NT immunoreactivity was also observed abundantly in airway inflammatory cells. In iNOS-deficient mice, both iNOS expression and NT formation were completely abolished, and the total amounts of nitrite and nitrate in BAL fluid were significantly decreased. In contrast, OVA-induced airway eosinophil recruitment and hyperresponsiveness were observed almost equally in wild-type and iNOS-deficient mice. These data suggest that reactive nitrogen species production after allergic reaction occurs totally via inducible nitric oxide synthase-dependent pathways. Allergen-mediated airway eosinophil recruitment and hyperresponsiveness appear to be independent of reactive nitrogen species production.</description><identifier>ISSN: 0903-1936</identifier><identifier>EISSN: 1399-3003</identifier><identifier>DOI: 10.1183/09031936.02.00274902</identifier><identifier>PMID: 12358336</identifier><language>eng</language><publisher>Leeds: Eur Respiratory Soc</publisher><subject>Allergens ; Allergic diseases ; Animals ; Biological and medical sciences ; Bronchi - pathology ; Bronchial Provocation Tests ; Bronchoalveolar Lavage Fluid - chemistry ; Bronchoalveolar Lavage Fluid - cytology ; Eosinophils - pathology ; Immunization ; Immunohistochemistry ; Immunopathology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitrates - analysis ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase - physiology ; Nitric Oxide Synthase Type II ; Nitrites - analysis ; Ovalbumin ; Reactive Nitrogen Species - metabolism ; Respiratory and ent allergic diseases ; Respiratory Hypersensitivity - immunology ; Respiratory Hypersensitivity - metabolism ; Respiratory Hypersensitivity - pathology ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism</subject><ispartof>The European respiratory journal, 2002-09, Vol.20 (3), p.609-616</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-e28e343e2858a9fdfb1509febec0f054d90fa68ac97335b873b5218fd5b091a43</citedby><cites>FETCH-LOGICAL-c475t-e28e343e2858a9fdfb1509febec0f054d90fa68ac97335b873b5218fd5b091a43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13901168$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12358336$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koarai, A</creatorcontrib><creatorcontrib>Ichinose, M</creatorcontrib><creatorcontrib>Sugiura, H</creatorcontrib><creatorcontrib>Tomaki, M</creatorcontrib><creatorcontrib>Watanabe, M</creatorcontrib><creatorcontrib>Yamagata, S</creatorcontrib><creatorcontrib>Komaki, Y</creatorcontrib><creatorcontrib>Shirato, K</creatorcontrib><creatorcontrib>Hattori, T</creatorcontrib><title>iNOS depletion completely diminishes reactive nitrogen-species formation after an allergic response</title><title>The European respiratory journal</title><addtitle>Eur Respir J</addtitle><description>Nitric oxide (NO) shows proinflammatory actions mainly via reactive nitrogen species (RNS) formation through superoxide- and peroxidase-dependent mechanisms. The purpose of this study was to examine the role of inducible NO synthase (iNOS) in RNS production, airway hyperresponsiveness, and inflammation after allergen challenge. Ovalbumin (OVA)-sensitised, iNOS-deficient and wild-type mice were used. RNS production was assessed by nitrotyrosine (NT) immunoreactivity in the airways. Airway inflammation and responsiveness were evaluated by eosinophil accumulation and methacholine (i.v.) challenge, respectively. In wild-type mice, OVA-inhalation challenge increased iNOS immunoreactivity in airway epithelial cells as well as iNOS protein measured by Western blotting. The total amounts of nitrite and nitrate in bronchoalveolar lavage (BAL) fluid were increased, and NT immunoreactivity was also observed abundantly in airway inflammatory cells. In iNOS-deficient mice, both iNOS expression and NT formation were completely abolished, and the total amounts of nitrite and nitrate in BAL fluid were significantly decreased. In contrast, OVA-induced airway eosinophil recruitment and hyperresponsiveness were observed almost equally in wild-type and iNOS-deficient mice. These data suggest that reactive nitrogen species production after allergic reaction occurs totally via inducible nitric oxide synthase-dependent pathways. Allergen-mediated airway eosinophil recruitment and hyperresponsiveness appear to be independent of reactive nitrogen species production.</description><subject>Allergens</subject><subject>Allergic diseases</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bronchi - pathology</subject><subject>Bronchial Provocation Tests</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>Eosinophils - pathology</subject><subject>Immunization</subject><subject>Immunohistochemistry</subject><subject>Immunopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nitrates - analysis</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase - physiology</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitrites - analysis</subject><subject>Ovalbumin</subject><subject>Reactive Nitrogen Species - metabolism</subject><subject>Respiratory and ent allergic diseases</subject><subject>Respiratory Hypersensitivity - immunology</subject><subject>Respiratory Hypersensitivity - metabolism</subject><subject>Respiratory Hypersensitivity - pathology</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><issn>0903-1936</issn><issn>1399-3003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1v1DAQhi0EokvhHyCUC9yyzHjiJD6iqlCkih6As-U4411X-cLOFvXf46Vb7WleaZ73PTxCvEfYIrb0GTQQaqq3ILcAsqk0yBdig6R1SQD0UmyOSHlkLsSblO4BsK4IX4sLlKRaonojXPhx97PoeRl4DfNUuHk8Rh4eiz6MYQppz6mIbN0aHriYwhrnHU9lWtiF_PFzHO3_pvUrx8LmMAwcd8HlVlrmKfFb8crbIfG7070Uv79e_7q6KW_vvn2_-nJbuqpRa8myZaooH9Va7XvfoQLtuWMHHlTVa_C2bq3TDZHq2oY6JbH1vepAo63oUnx62l3i_OfAaTVjSI6HwU48H5JpJBIRqgxWT6CLc0qRvVliGG18NAjmKNc8yzUgzbPcXPtw2j90I_fn0slmBj6eAJucHXy0kwvpzJEGxLo9c_uw2_8NkU0as7U8i4bjvQRDpgZN_wB6eJAl</recordid><startdate>20020901</startdate><enddate>20020901</enddate><creator>Koarai, A</creator><creator>Ichinose, M</creator><creator>Sugiura, H</creator><creator>Tomaki, M</creator><creator>Watanabe, M</creator><creator>Yamagata, S</creator><creator>Komaki, Y</creator><creator>Shirato, K</creator><creator>Hattori, T</creator><general>Eur Respiratory Soc</general><general>Maney</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>20020901</creationdate><title>iNOS depletion completely diminishes reactive nitrogen-species formation after an allergic response</title><author>Koarai, A ; Ichinose, M ; Sugiura, H ; Tomaki, M ; Watanabe, M ; Yamagata, S ; Komaki, Y ; Shirato, K ; Hattori, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-e28e343e2858a9fdfb1509febec0f054d90fa68ac97335b873b5218fd5b091a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Allergens</topic><topic>Allergic diseases</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bronchi - pathology</topic><topic>Bronchial Provocation Tests</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Bronchoalveolar Lavage Fluid - cytology</topic><topic>Eosinophils - pathology</topic><topic>Immunization</topic><topic>Immunohistochemistry</topic><topic>Immunopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nitrates - analysis</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase - physiology</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nitrites - analysis</topic><topic>Ovalbumin</topic><topic>Reactive Nitrogen Species - metabolism</topic><topic>Respiratory and ent allergic diseases</topic><topic>Respiratory Hypersensitivity - immunology</topic><topic>Respiratory Hypersensitivity - metabolism</topic><topic>Respiratory Hypersensitivity - pathology</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koarai, A</creatorcontrib><creatorcontrib>Ichinose, M</creatorcontrib><creatorcontrib>Sugiura, H</creatorcontrib><creatorcontrib>Tomaki, M</creatorcontrib><creatorcontrib>Watanabe, M</creatorcontrib><creatorcontrib>Yamagata, S</creatorcontrib><creatorcontrib>Komaki, Y</creatorcontrib><creatorcontrib>Shirato, K</creatorcontrib><creatorcontrib>Hattori, T</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>The European respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koarai, A</au><au>Ichinose, M</au><au>Sugiura, H</au><au>Tomaki, M</au><au>Watanabe, M</au><au>Yamagata, S</au><au>Komaki, Y</au><au>Shirato, K</au><au>Hattori, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>iNOS depletion completely diminishes reactive nitrogen-species formation after an allergic response</atitle><jtitle>The European respiratory journal</jtitle><addtitle>Eur Respir J</addtitle><date>2002-09-01</date><risdate>2002</risdate><volume>20</volume><issue>3</issue><spage>609</spage><epage>616</epage><pages>609-616</pages><issn>0903-1936</issn><eissn>1399-3003</eissn><abstract>Nitric oxide (NO) shows proinflammatory actions mainly via reactive nitrogen species (RNS) formation through superoxide- and peroxidase-dependent mechanisms. The purpose of this study was to examine the role of inducible NO synthase (iNOS) in RNS production, airway hyperresponsiveness, and inflammation after allergen challenge. Ovalbumin (OVA)-sensitised, iNOS-deficient and wild-type mice were used. RNS production was assessed by nitrotyrosine (NT) immunoreactivity in the airways. Airway inflammation and responsiveness were evaluated by eosinophil accumulation and methacholine (i.v.) challenge, respectively. In wild-type mice, OVA-inhalation challenge increased iNOS immunoreactivity in airway epithelial cells as well as iNOS protein measured by Western blotting. The total amounts of nitrite and nitrate in bronchoalveolar lavage (BAL) fluid were increased, and NT immunoreactivity was also observed abundantly in airway inflammatory cells. In iNOS-deficient mice, both iNOS expression and NT formation were completely abolished, and the total amounts of nitrite and nitrate in BAL fluid were significantly decreased. In contrast, OVA-induced airway eosinophil recruitment and hyperresponsiveness were observed almost equally in wild-type and iNOS-deficient mice. These data suggest that reactive nitrogen species production after allergic reaction occurs totally via inducible nitric oxide synthase-dependent pathways. Allergen-mediated airway eosinophil recruitment and hyperresponsiveness appear to be independent of reactive nitrogen species production.</abstract><cop>Leeds</cop><pub>Eur Respiratory Soc</pub><pmid>12358336</pmid><doi>10.1183/09031936.02.00274902</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergens Allergic diseases Animals Biological and medical sciences Bronchi - pathology Bronchial Provocation Tests Bronchoalveolar Lavage Fluid - chemistry Bronchoalveolar Lavage Fluid - cytology Eosinophils - pathology Immunization Immunohistochemistry Immunopathology Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Nitrates - analysis Nitric Oxide Synthase - metabolism Nitric Oxide Synthase - physiology Nitric Oxide Synthase Type II Nitrites - analysis Ovalbumin Reactive Nitrogen Species - metabolism Respiratory and ent allergic diseases Respiratory Hypersensitivity - immunology Respiratory Hypersensitivity - metabolism Respiratory Hypersensitivity - pathology Tyrosine - analogs & derivatives Tyrosine - metabolism |
| title | iNOS depletion completely diminishes reactive nitrogen-species formation after an allergic response |
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