Signal transducer and activator of transcription 6 (STAT-6) expression and function in asthmatic bronchial epithelium
Background: Asthma is associated with increased production of IL-4 and IL-13. Objective: Because many of the effects of these cytokines are mediated by activation of signal transducer and activator of transcription 6 (STAT-6), we investigated expression and function of this transcription factor in t...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 2001-11, Vol.108 (5), p.832-838 |
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| creator | Mullings, Rebecca E. Wilson, Susan J. Puddicombe, Sarah M. Lordan, James L. Bucchieri, Fabio Djukanović, Ratko Howarth, Peter H. Harper, Steven Holgate, Stephen T. Davies, Donna E. |
| description | Background: Asthma is associated with increased production of IL-4 and IL-13. Objective: Because many of the effects of these cytokines are mediated by activation of signal transducer and activator of transcription 6 (STAT-6), we investigated expression and function of this transcription factor in the airways. Methods: STAT-6 expression was investigated through use of immunohistochemistry or RT-PCR applied to bronchial biopsy specimens or brushings from normal control or asthmatic subjects. STAT-6 function was investigated by means of Western blotting and ELISA applied to primary epithelial cell cultures. Results: Immunohistochemistry revealed that the bronchial epithelium was the major site of STAT-6 expression, both cytoplasmic and nuclear staining being observed. The level of STAT-6 expression in subjects with mild asthma (median [range] percent epithelial staining, 3.4% [0% to 16.0%]; n = 14) did not differ significantly from that in normal controls (4.7% [0.0% to 20.0%]; n = 11); however, in subjects with severe asthma, epithelial STAT-6 expression (13.7% [4.8% to 25.7%]; n = 9) was increased in comparison with subjects with mild asthma and normal controls (P < .05). RT-PCR analysis showed that epithelial STAT-6 expression was heterogeneous and comprised both full-length STAT-6 and the dominant-negative variant that lacks the SH2 domain. Treatment of primary cultures of bronchial epithelial cells with IL-4 resulted in STAT-6 phosphorylation and stimulation of IL-8 secretion; however, no difference in the responses of epithelial cells was observed between normal (n = 12) and asthmatic (n = 14) donors. Conclusion: These data demonstrate expression and activation of STAT-6 in normal and asthmatic bronchial epithelium. The activity of this transcription factor is likely to play a key role in mediating the responses of the bronchial epithelium to TH2 cytokines that are characteristic of the asthmatic phenotype. (J Allergy Clin Immunol 2001;108:832-8.) |
| doi_str_mv | 10.1067/mai.2001.119554 |
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Objective: Because many of the effects of these cytokines are mediated by activation of signal transducer and activator of transcription 6 (STAT-6), we investigated expression and function of this transcription factor in the airways. Methods: STAT-6 expression was investigated through use of immunohistochemistry or RT-PCR applied to bronchial biopsy specimens or brushings from normal control or asthmatic subjects. STAT-6 function was investigated by means of Western blotting and ELISA applied to primary epithelial cell cultures. Results: Immunohistochemistry revealed that the bronchial epithelium was the major site of STAT-6 expression, both cytoplasmic and nuclear staining being observed. The level of STAT-6 expression in subjects with mild asthma (median [range] percent epithelial staining, 3.4% [0% to 16.0%]; n = 14) did not differ significantly from that in normal controls (4.7% [0.0% to 20.0%]; n = 11); however, in subjects with severe asthma, epithelial STAT-6 expression (13.7% [4.8% to 25.7%]; n = 9) was increased in comparison with subjects with mild asthma and normal controls (P < .05). RT-PCR analysis showed that epithelial STAT-6 expression was heterogeneous and comprised both full-length STAT-6 and the dominant-negative variant that lacks the SH2 domain. Treatment of primary cultures of bronchial epithelial cells with IL-4 resulted in STAT-6 phosphorylation and stimulation of IL-8 secretion; however, no difference in the responses of epithelial cells was observed between normal (n = 12) and asthmatic (n = 14) donors. Conclusion: These data demonstrate expression and activation of STAT-6 in normal and asthmatic bronchial epithelium. The activity of this transcription factor is likely to play a key role in mediating the responses of the bronchial epithelium to TH2 cytokines that are characteristic of the asthmatic phenotype. (J Allergy Clin Immunol 2001;108:832-8.)</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1067/mai.2001.119554</identifier><identifier>PMID: 11692112</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Allergic diseases ; Asthma ; Asthma - immunology ; Biological and medical sciences ; Bronchi - cytology ; Cells, Cultured ; epithelium ; Humans ; IL-13 ; IL-4 ; IL-8 ; Immunohistochemistry ; Immunopathology ; Interleukin-13 - pharmacology ; Interleukin-4 - pharmacology ; Interleukin-8 - biosynthesis ; Janus Kinase 1 ; Medical sciences ; Models, Biological ; Phosphorylation ; Protein-Tyrosine Kinases - metabolism ; Respiratory and ent allergic diseases ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - immunology ; RNA, Messenger - biosynthesis ; STAT-6 ; Stat6 protein ; STAT6 Transcription Factor ; TH2 ; Trans-Activators - biosynthesis ; Trans-Activators - genetics ; Trans-Activators - physiology ; Transcription, Genetic</subject><ispartof>Journal of allergy and clinical immunology, 2001-11, Vol.108 (5), p.832-838</ispartof><rights>2001 Mosby, Inc.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-915839fe04fcd01f54580f1ee20d2c274c1b3fdf9d3ba7e1e06b0fa6ae9cc70c3</citedby><cites>FETCH-LOGICAL-c511t-915839fe04fcd01f54580f1ee20d2c274c1b3fdf9d3ba7e1e06b0fa6ae9cc70c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1067/mai.2001.119554$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13393520$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11692112$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mullings, Rebecca E.</creatorcontrib><creatorcontrib>Wilson, Susan J.</creatorcontrib><creatorcontrib>Puddicombe, Sarah M.</creatorcontrib><creatorcontrib>Lordan, James L.</creatorcontrib><creatorcontrib>Bucchieri, Fabio</creatorcontrib><creatorcontrib>Djukanović, Ratko</creatorcontrib><creatorcontrib>Howarth, Peter H.</creatorcontrib><creatorcontrib>Harper, Steven</creatorcontrib><creatorcontrib>Holgate, Stephen T.</creatorcontrib><creatorcontrib>Davies, Donna E.</creatorcontrib><title>Signal transducer and activator of transcription 6 (STAT-6) expression and function in asthmatic bronchial epithelium</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Background: Asthma is associated with increased production of IL-4 and IL-13. Objective: Because many of the effects of these cytokines are mediated by activation of signal transducer and activator of transcription 6 (STAT-6), we investigated expression and function of this transcription factor in the airways. Methods: STAT-6 expression was investigated through use of immunohistochemistry or RT-PCR applied to bronchial biopsy specimens or brushings from normal control or asthmatic subjects. STAT-6 function was investigated by means of Western blotting and ELISA applied to primary epithelial cell cultures. Results: Immunohistochemistry revealed that the bronchial epithelium was the major site of STAT-6 expression, both cytoplasmic and nuclear staining being observed. The level of STAT-6 expression in subjects with mild asthma (median [range] percent epithelial staining, 3.4% [0% to 16.0%]; n = 14) did not differ significantly from that in normal controls (4.7% [0.0% to 20.0%]; n = 11); however, in subjects with severe asthma, epithelial STAT-6 expression (13.7% [4.8% to 25.7%]; n = 9) was increased in comparison with subjects with mild asthma and normal controls (P < .05). RT-PCR analysis showed that epithelial STAT-6 expression was heterogeneous and comprised both full-length STAT-6 and the dominant-negative variant that lacks the SH2 domain. Treatment of primary cultures of bronchial epithelial cells with IL-4 resulted in STAT-6 phosphorylation and stimulation of IL-8 secretion; however, no difference in the responses of epithelial cells was observed between normal (n = 12) and asthmatic (n = 14) donors. Conclusion: These data demonstrate expression and activation of STAT-6 in normal and asthmatic bronchial epithelium. The activity of this transcription factor is likely to play a key role in mediating the responses of the bronchial epithelium to TH2 cytokines that are characteristic of the asthmatic phenotype. (J Allergy Clin Immunol 2001;108:832-8.)</description><subject>Allergic diseases</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Biological and medical sciences</subject><subject>Bronchi - cytology</subject><subject>Cells, Cultured</subject><subject>epithelium</subject><subject>Humans</subject><subject>IL-13</subject><subject>IL-4</subject><subject>IL-8</subject><subject>Immunohistochemistry</subject><subject>Immunopathology</subject><subject>Interleukin-13 - pharmacology</subject><subject>Interleukin-4 - pharmacology</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Janus Kinase 1</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Phosphorylation</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Respiratory and ent allergic diseases</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - immunology</subject><subject>RNA, Messenger - biosynthesis</subject><subject>STAT-6</subject><subject>Stat6 protein</subject><subject>STAT6 Transcription Factor</subject><subject>TH2</subject><subject>Trans-Activators - biosynthesis</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - physiology</subject><subject>Transcription, Genetic</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUuP1DAMgCMEYoeFMzfUCwgOnY2Tpm2OqxUvaSUOO5yj1HWYoL5I0hX778nQkfaEOFl2PtuRP8ZeA98Dr5ur0fq94Bz2AFqp6gnbAddNWbdCPWU7zjWUdVPpC_Yixp8857LVz9kFQK0FgNix9c7_mOxQpGCn2K9IobBTX1hM_t6mORSz294w-CX5eSrq4v3d4fpQ1h8K-r0EivFUPTW5dcK_iM95TMfRJo9FF-YJjz7voMWnIw1-HV-yZ84OkV6d4yX7_unj4eZLefvt89eb69sSFUAqNahWake8cthzcKpSLXdAJHgvUDQVQidd73QvO9sQEK877mxtSSM2HOUle7fNXcL8a6WYzOgj0jDYieY1mkYI1XCA_4LQSiUVyAxebSCGOcZAzizBjzY8GODmpMRkJeakxGxKcseb8-i1G6l_5M8OMvD2DNiIdnD52ujjIyellkrwzOmNo3yxe0_BRPQ0IfU-ECbTz_6fn_gDb3CozA</recordid><startdate>20011101</startdate><enddate>20011101</enddate><creator>Mullings, Rebecca E.</creator><creator>Wilson, Susan J.</creator><creator>Puddicombe, Sarah M.</creator><creator>Lordan, James L.</creator><creator>Bucchieri, Fabio</creator><creator>Djukanović, Ratko</creator><creator>Howarth, Peter H.</creator><creator>Harper, Steven</creator><creator>Holgate, Stephen T.</creator><creator>Davies, Donna E.</creator><general>Mosby, Inc</general><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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20011101</creationdate><title>Signal transducer and activator of transcription 6 (STAT-6) expression and function in asthmatic bronchial epithelium</title><author>Mullings, Rebecca E. ; Wilson, Susan J. ; Puddicombe, Sarah M. ; Lordan, James L. ; Bucchieri, Fabio ; Djukanović, Ratko ; Howarth, Peter H. ; Harper, Steven ; Holgate, Stephen T. ; Davies, Donna E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-915839fe04fcd01f54580f1ee20d2c274c1b3fdf9d3ba7e1e06b0fa6ae9cc70c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Allergic diseases</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Biological and medical sciences</topic><topic>Bronchi - cytology</topic><topic>Cells, Cultured</topic><topic>epithelium</topic><topic>Humans</topic><topic>IL-13</topic><topic>IL-4</topic><topic>IL-8</topic><topic>Immunohistochemistry</topic><topic>Immunopathology</topic><topic>Interleukin-13 - pharmacology</topic><topic>Interleukin-4 - pharmacology</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Janus Kinase 1</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Phosphorylation</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Respiratory and ent allergic diseases</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - immunology</topic><topic>RNA, Messenger - biosynthesis</topic><topic>STAT-6</topic><topic>Stat6 protein</topic><topic>STAT6 Transcription Factor</topic><topic>TH2</topic><topic>Trans-Activators - biosynthesis</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - physiology</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mullings, Rebecca E.</creatorcontrib><creatorcontrib>Wilson, Susan J.</creatorcontrib><creatorcontrib>Puddicombe, Sarah M.</creatorcontrib><creatorcontrib>Lordan, James L.</creatorcontrib><creatorcontrib>Bucchieri, Fabio</creatorcontrib><creatorcontrib>Djukanović, Ratko</creatorcontrib><creatorcontrib>Howarth, Peter H.</creatorcontrib><creatorcontrib>Harper, Steven</creatorcontrib><creatorcontrib>Holgate, Stephen T.</creatorcontrib><creatorcontrib>Davies, Donna E.</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</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>Mullings, Rebecca E.</au><au>Wilson, Susan J.</au><au>Puddicombe, Sarah M.</au><au>Lordan, James L.</au><au>Bucchieri, Fabio</au><au>Djukanović, Ratko</au><au>Howarth, Peter H.</au><au>Harper, Steven</au><au>Holgate, Stephen T.</au><au>Davies, Donna E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Signal transducer and activator of transcription 6 (STAT-6) expression and function in asthmatic bronchial epithelium</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2001-11-01</date><risdate>2001</risdate><volume>108</volume><issue>5</issue><spage>832</spage><epage>838</epage><pages>832-838</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Background: Asthma is associated with increased production of IL-4 and IL-13. Objective: Because many of the effects of these cytokines are mediated by activation of signal transducer and activator of transcription 6 (STAT-6), we investigated expression and function of this transcription factor in the airways. Methods: STAT-6 expression was investigated through use of immunohistochemistry or RT-PCR applied to bronchial biopsy specimens or brushings from normal control or asthmatic subjects. STAT-6 function was investigated by means of Western blotting and ELISA applied to primary epithelial cell cultures. Results: Immunohistochemistry revealed that the bronchial epithelium was the major site of STAT-6 expression, both cytoplasmic and nuclear staining being observed. The level of STAT-6 expression in subjects with mild asthma (median [range] percent epithelial staining, 3.4% [0% to 16.0%]; n = 14) did not differ significantly from that in normal controls (4.7% [0.0% to 20.0%]; n = 11); however, in subjects with severe asthma, epithelial STAT-6 expression (13.7% [4.8% to 25.7%]; n = 9) was increased in comparison with subjects with mild asthma and normal controls (P < .05). RT-PCR analysis showed that epithelial STAT-6 expression was heterogeneous and comprised both full-length STAT-6 and the dominant-negative variant that lacks the SH2 domain. Treatment of primary cultures of bronchial epithelial cells with IL-4 resulted in STAT-6 phosphorylation and stimulation of IL-8 secretion; however, no difference in the responses of epithelial cells was observed between normal (n = 12) and asthmatic (n = 14) donors. Conclusion: These data demonstrate expression and activation of STAT-6 in normal and asthmatic bronchial epithelium. The activity of this transcription factor is likely to play a key role in mediating the responses of the bronchial epithelium to TH2 cytokines that are characteristic of the asthmatic phenotype. (J Allergy Clin Immunol 2001;108:832-8.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>11692112</pmid><doi>10.1067/mai.2001.119554</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergic diseases Asthma Asthma - immunology Biological and medical sciences Bronchi - cytology Cells, Cultured epithelium Humans IL-13 IL-4 IL-8 Immunohistochemistry Immunopathology Interleukin-13 - pharmacology Interleukin-4 - pharmacology Interleukin-8 - biosynthesis Janus Kinase 1 Medical sciences Models, Biological Phosphorylation Protein-Tyrosine Kinases - metabolism Respiratory and ent allergic diseases Respiratory Mucosa - drug effects Respiratory Mucosa - immunology RNA, Messenger - biosynthesis STAT-6 Stat6 protein STAT6 Transcription Factor TH2 Trans-Activators - biosynthesis Trans-Activators - genetics Trans-Activators - physiology Transcription, Genetic |
| title | Signal transducer and activator of transcription 6 (STAT-6) expression and function in asthmatic bronchial epithelium |
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