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Expression and function of the ST2 gene in a murine model of allergic airway inflammation
Summary Background We have recently reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation. However, the role, function, and kinetics of soluble ST2 expression in asthma remain unclear. Objective The obje...
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| Published in: | Clinical and experimental allergy 2002-10, Vol.32 (10), p.1520-1526 |
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| container_title | Clinical and experimental allergy |
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| creator | Oshikawa, K. Yanagisawa, K. Tominaga, S. Sugiyama, Y. |
| description | Summary
Background We have recently reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation. However, the role, function, and kinetics of soluble ST2 expression in asthma remain unclear.
Objective The objective of the present study was to clarify the function and kinetics of soluble murine (m) ST2 expression in a murine asthma model.
Methods We analyzed the kinetics of gene and protein expression of mST2 in sera or lung tissue after allergen (ovalbumin; OVA) challenge in a murine model of allergic airway inflammation, the effects of mST2 protein on OVA‐induced Th2 cytokine production in vitro from splenocytes of sensitized mice, and the effects of soluble mST2 on Th2‐dependent allergic airway inflammation by in vivo gene transfer of mST2.
Results Serum mST2 protein levels increased to the maximal level 3 h after the allergen challenge, before serum IL‐5 levels peaked. The mRNA expression of mST2 in lung tissue was induced after the allergen challenge, while that in the spleen was constitutively detected. Furthermore, pre‐treatment with mST2 protein significantly inhibited the production of IL‐4 and IL‐5, but not IFN‐γ, from OVA‐stimulated splenocytes in vitro, and intravenous mST2 gene transfer resulted in a drastic reduction in the number of eosinophils and in the levels of IL‐4 and IL‐5 in bronchoalveolar lavage fluid, compared with those in response to transfer of non‐coding plasmid vector or of lipid alone.
Conclusion These results suggest that increases in endogenous mST2 protein after allergen exposure may modulate Th2‐mediated airway inflammation, and that in vivo gene transfer of mST2 can be applicable to use in a novel immunotherapy for allergic diseases. |
| doi_str_mv | 10.1046/j.1365-2745.2002.01494.x |
| format | article |
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Background We have recently reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation. However, the role, function, and kinetics of soluble ST2 expression in asthma remain unclear.
Objective The objective of the present study was to clarify the function and kinetics of soluble murine (m) ST2 expression in a murine asthma model.
Methods We analyzed the kinetics of gene and protein expression of mST2 in sera or lung tissue after allergen (ovalbumin; OVA) challenge in a murine model of allergic airway inflammation, the effects of mST2 protein on OVA‐induced Th2 cytokine production in vitro from splenocytes of sensitized mice, and the effects of soluble mST2 on Th2‐dependent allergic airway inflammation by in vivo gene transfer of mST2.
Results Serum mST2 protein levels increased to the maximal level 3 h after the allergen challenge, before serum IL‐5 levels peaked. The mRNA expression of mST2 in lung tissue was induced after the allergen challenge, while that in the spleen was constitutively detected. Furthermore, pre‐treatment with mST2 protein significantly inhibited the production of IL‐4 and IL‐5, but not IFN‐γ, from OVA‐stimulated splenocytes in vitro, and intravenous mST2 gene transfer resulted in a drastic reduction in the number of eosinophils and in the levels of IL‐4 and IL‐5 in bronchoalveolar lavage fluid, compared with those in response to transfer of non‐coding plasmid vector or of lipid alone.
Conclusion These results suggest that increases in endogenous mST2 protein after allergen exposure may modulate Th2‐mediated airway inflammation, and that in vivo gene transfer of mST2 can be applicable to use in a novel immunotherapy for allergic diseases.</description><identifier>ISSN: 0954-7894</identifier><identifier>EISSN: 1365-2222</identifier><identifier>DOI: 10.1046/j.1365-2745.2002.01494.x</identifier><identifier>PMID: 12372135</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science, Ltd</publisher><subject>Allergens ; Allergic diseases ; allergy ; Analysis of Variance ; Animals ; asthma ; Biological and medical sciences ; Bronchoalveolar Lavage Fluid - immunology ; Female ; Gene Expression ; gene therapy ; Genetic Engineering ; Genetic Vectors - administration & dosage ; Immunopathology ; Interferon-gamma - blood ; Interleukin-1 Receptor-Like 1 Protein ; Interleukin-4 - blood ; Interleukin-5 - blood ; Lung - metabolism ; Medical sciences ; Membrane Proteins - blood ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred BALB C ; Models, Animal ; Ovalbumin ; Receptors, Interleukin ; Respiratory and ent allergic diseases ; Respiratory Hypersensitivity - metabolism ; T1/ST2 ; type-2 helper T cell</subject><ispartof>Clinical and experimental allergy, 2002-10, Vol.32 (10), p.1520-1526</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Oct 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6074-8012edd2cf7c8b91d6ec5a36ac3c605289392c26d8053180f5aad40a7812d2983</citedby><cites>FETCH-LOGICAL-c6074-8012edd2cf7c8b91d6ec5a36ac3c605289392c26d8053180f5aad40a7812d2983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2745.2002.01494.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2745.2002.01494.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13956337$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12372135$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oshikawa, K.</creatorcontrib><creatorcontrib>Yanagisawa, K.</creatorcontrib><creatorcontrib>Tominaga, S.</creatorcontrib><creatorcontrib>Sugiyama, Y.</creatorcontrib><title>Expression and function of the ST2 gene in a murine model of allergic airway inflammation</title><title>Clinical and experimental allergy</title><addtitle>Clin Exp Allergy</addtitle><description>Summary
Background We have recently reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation. However, the role, function, and kinetics of soluble ST2 expression in asthma remain unclear.
Objective The objective of the present study was to clarify the function and kinetics of soluble murine (m) ST2 expression in a murine asthma model.
Methods We analyzed the kinetics of gene and protein expression of mST2 in sera or lung tissue after allergen (ovalbumin; OVA) challenge in a murine model of allergic airway inflammation, the effects of mST2 protein on OVA‐induced Th2 cytokine production in vitro from splenocytes of sensitized mice, and the effects of soluble mST2 on Th2‐dependent allergic airway inflammation by in vivo gene transfer of mST2.
Results Serum mST2 protein levels increased to the maximal level 3 h after the allergen challenge, before serum IL‐5 levels peaked. The mRNA expression of mST2 in lung tissue was induced after the allergen challenge, while that in the spleen was constitutively detected. Furthermore, pre‐treatment with mST2 protein significantly inhibited the production of IL‐4 and IL‐5, but not IFN‐γ, from OVA‐stimulated splenocytes in vitro, and intravenous mST2 gene transfer resulted in a drastic reduction in the number of eosinophils and in the levels of IL‐4 and IL‐5 in bronchoalveolar lavage fluid, compared with those in response to transfer of non‐coding plasmid vector or of lipid alone.
Conclusion These results suggest that increases in endogenous mST2 protein after allergen exposure may modulate Th2‐mediated airway inflammation, and that in vivo gene transfer of mST2 can be applicable to use in a novel immunotherapy for allergic diseases.</description><subject>Allergens</subject><subject>Allergic diseases</subject><subject>allergy</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>asthma</subject><subject>Biological and medical sciences</subject><subject>Bronchoalveolar Lavage Fluid - immunology</subject><subject>Female</subject><subject>Gene Expression</subject><subject>gene therapy</subject><subject>Genetic Engineering</subject><subject>Genetic Vectors - administration & dosage</subject><subject>Immunopathology</subject><subject>Interferon-gamma - blood</subject><subject>Interleukin-1 Receptor-Like 1 Protein</subject><subject>Interleukin-4 - blood</subject><subject>Interleukin-5 - blood</subject><subject>Lung - metabolism</subject><subject>Medical sciences</subject><subject>Membrane Proteins - blood</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Models, Animal</subject><subject>Ovalbumin</subject><subject>Receptors, Interleukin</subject><subject>Respiratory and ent allergic diseases</subject><subject>Respiratory Hypersensitivity - metabolism</subject><subject>T1/ST2</subject><subject>type-2 helper T cell</subject><issn>0954-7894</issn><issn>1365-2222</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqNksluFDEQhi0EIkPgFZCFBLduvLS3A4dkNNkUgQRBiJPl2O7goZfBnlZm3h47PSISF_DFVarvL1X5NwAQoxqjhr9f15hyVhHRsJogRGqEG9XUuydgMRfyeQoWSLGmElI1R-BFSmuEEGVKPgdHmFBBMGUL8H2120SfUhgHaAYH22mw25KMLdz-8PDLDYF3fvAw5Drspxhy3I_Od4UwXefjXbDQhHhv9hlqO9P3pnR4CZ61pkv-1eE-Bl_PVjfLi-r60_nl8uS6shyJppIIE-8csa2w8lZhx71lhnJjaQYYkYoqYgl3EjGKJWqZMa5BRkhMHFGSHoN3c99NHH9NPm11H5L1XWcGP05J50W5yi_1TxBLQYgSIoNv_gLX4xSHvITGSklOuEIZkjNk45hS9K3exNCbuNcY6WKSXuvihS4m6WKSfjBJ77L09aH_dNt79yg8uJKBtwfAJGu6NprBhvTIUcU4pWXQDzN3Hzq__-8B9HJ1UqKsr2Z9SFu_-6M38afmggqmv3081_nPXJ1efD7TV_Q3WMi5-w</recordid><startdate>200210</startdate><enddate>200210</enddate><creator>Oshikawa, K.</creator><creator>Yanagisawa, K.</creator><creator>Tominaga, S.</creator><creator>Sugiyama, Y.</creator><general>Blackwell Science, Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>200210</creationdate><title>Expression and function of the ST2 gene in a murine model of allergic airway inflammation</title><author>Oshikawa, K. ; Yanagisawa, K. ; Tominaga, S. ; Sugiyama, Y.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6074-8012edd2cf7c8b91d6ec5a36ac3c605289392c26d8053180f5aad40a7812d2983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Allergens</topic><topic>Allergic diseases</topic><topic>allergy</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>asthma</topic><topic>Biological and medical sciences</topic><topic>Bronchoalveolar Lavage Fluid - immunology</topic><topic>Female</topic><topic>Gene Expression</topic><topic>gene therapy</topic><topic>Genetic Engineering</topic><topic>Genetic Vectors - administration & dosage</topic><topic>Immunopathology</topic><topic>Interferon-gamma - blood</topic><topic>Interleukin-1 Receptor-Like 1 Protein</topic><topic>Interleukin-4 - blood</topic><topic>Interleukin-5 - blood</topic><topic>Lung - metabolism</topic><topic>Medical sciences</topic><topic>Membrane Proteins - blood</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Models, Animal</topic><topic>Ovalbumin</topic><topic>Receptors, Interleukin</topic><topic>Respiratory and ent allergic diseases</topic><topic>Respiratory Hypersensitivity - metabolism</topic><topic>T1/ST2</topic><topic>type-2 helper T cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oshikawa, K.</creatorcontrib><creatorcontrib>Yanagisawa, K.</creatorcontrib><creatorcontrib>Tominaga, S.</creatorcontrib><creatorcontrib>Sugiyama, Y.</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental allergy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oshikawa, K.</au><au>Yanagisawa, K.</au><au>Tominaga, S.</au><au>Sugiyama, Y.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression and function of the ST2 gene in a murine model of allergic airway inflammation</atitle><jtitle>Clinical and experimental allergy</jtitle><addtitle>Clin Exp Allergy</addtitle><date>2002-10</date><risdate>2002</risdate><volume>32</volume><issue>10</issue><spage>1520</spage><epage>1526</epage><pages>1520-1526</pages><issn>0954-7894</issn><eissn>1365-2222</eissn><notes>ark:/67375/WNG-035JBHRF-J</notes><notes>istex:4028E316A0DD1ED39E0E969DEEAF5D57713104A5</notes><notes>ArticleID:CEA1494</notes><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><notes>ObjectType-Article-1</notes><notes>ObjectType-Feature-2</notes><abstract>Summary
Background We have recently reported that soluble ST2 protein levels are elevated in the sera of patients with asthma, and correlate well with the severity of asthma exacerbation. However, the role, function, and kinetics of soluble ST2 expression in asthma remain unclear.
Objective The objective of the present study was to clarify the function and kinetics of soluble murine (m) ST2 expression in a murine asthma model.
Methods We analyzed the kinetics of gene and protein expression of mST2 in sera or lung tissue after allergen (ovalbumin; OVA) challenge in a murine model of allergic airway inflammation, the effects of mST2 protein on OVA‐induced Th2 cytokine production in vitro from splenocytes of sensitized mice, and the effects of soluble mST2 on Th2‐dependent allergic airway inflammation by in vivo gene transfer of mST2.
Results Serum mST2 protein levels increased to the maximal level 3 h after the allergen challenge, before serum IL‐5 levels peaked. The mRNA expression of mST2 in lung tissue was induced after the allergen challenge, while that in the spleen was constitutively detected. Furthermore, pre‐treatment with mST2 protein significantly inhibited the production of IL‐4 and IL‐5, but not IFN‐γ, from OVA‐stimulated splenocytes in vitro, and intravenous mST2 gene transfer resulted in a drastic reduction in the number of eosinophils and in the levels of IL‐4 and IL‐5 in bronchoalveolar lavage fluid, compared with those in response to transfer of non‐coding plasmid vector or of lipid alone.
Conclusion These results suggest that increases in endogenous mST2 protein after allergen exposure may modulate Th2‐mediated airway inflammation, and that in vivo gene transfer of mST2 can be applicable to use in a novel immunotherapy for allergic diseases.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science, Ltd</pub><pmid>12372135</pmid><doi>10.1046/j.1365-2745.2002.01494.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergens Allergic diseases allergy Analysis of Variance Animals asthma Biological and medical sciences Bronchoalveolar Lavage Fluid - immunology Female Gene Expression gene therapy Genetic Engineering Genetic Vectors - administration & dosage Immunopathology Interferon-gamma - blood Interleukin-1 Receptor-Like 1 Protein Interleukin-4 - blood Interleukin-5 - blood Lung - metabolism Medical sciences Membrane Proteins - blood Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred BALB C Models, Animal Ovalbumin Receptors, Interleukin Respiratory and ent allergic diseases Respiratory Hypersensitivity - metabolism T1/ST2 type-2 helper T cell |
| title | Expression and function of the ST2 gene in a murine model of allergic airway inflammation |
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