Lack of inducible nitric oxide synthase in bronchial epithelium: a possible mechanism of susceptibility to infection in cystic fibrosis
Cystic fibrosis (CF) is an inherited disorder associated with severe inflammation and repeated bacterial infection and colonization in the lung. Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro‐inflammatory cytokines can stimulate the expression...
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| Veröffentlicht in: | The Journal of pathology 1998-03, Vol.184 (3), p.323-331 |
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| creator | Meng, Qing-Hai Springall, David R. Bishop, Anne E. Morgan, Kevin Evans, Tom J. Habib, Said Gruenert, Dieter C. Gyi, Khin M. Hodson, Margaret E. Yacoub, Magdi H. Polak, Julia M. |
| description | Cystic fibrosis (CF) is an inherited disorder associated with severe inflammation and repeated bacterial infection and colonization in the lung. Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro‐inflammatory cytokines can stimulate the expression of inducible nitric oxide synthase (iNOS), an enzyme generating nitric oxide, which functions as an important mediator in host defence mechanisms. To understand better the poor resistance to infections in the CF lung, the expression of the iNOS gene was investigated in explanted lungs from patients with cystic fibrosis (n‐13), bronchiectasis (n‐3), emphysema (n‐14), and in normal lungs (n‐8). In addition, bronchial epithelial cell lines were examined to study iNOS gene expression in vitro. Strong immunoreactivity for iNOS was seen in inflammatory cells and bronchial epithelium in all the diseased lungs, except for bronchial epithelium in CF. Quantitative analysis showed a significant reduction in the area of epithelium immunostained in CF [CF 6·8±1·6 (%±SEM); emphysema 18·2±2·8; normal 9·6±0·8, P |
| doi_str_mv | 10.1002/(SICI)1096-9896(199803)184:3<323::AID-PATH2>3.0.CO;2-2 |
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Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro‐inflammatory cytokines can stimulate the expression of inducible nitric oxide synthase (iNOS), an enzyme generating nitric oxide, which functions as an important mediator in host defence mechanisms. To understand better the poor resistance to infections in the CF lung, the expression of the iNOS gene was investigated in explanted lungs from patients with cystic fibrosis (n‐13), bronchiectasis (n‐3), emphysema (n‐14), and in normal lungs (n‐8). In addition, bronchial epithelial cell lines were examined to study iNOS gene expression in vitro. Strong immunoreactivity for iNOS was seen in inflammatory cells and bronchial epithelium in all the diseased lungs, except for bronchial epithelium in CF. Quantitative analysis showed a significant reduction in the area of epithelium immunostained in CF [CF 6·8±1·6 (%±SEM); emphysema 18·2±2·8; normal 9·6±0·8, P<0·01], regardless of steroid treatment. These results were supported by in situ hybridization of iNOS mRNA, which showed a pattern of gene expression in CF, emphysema, and normal lung which paralleled that of protein immunoreactivity. Stimulation with cytokines (IL‐1β, TNF‐α, and IFN‐γ) increased the expression of iNOS mRNA detected by reverse transcriptase‐polymerase chain reaction (RT‐PCR) in cultures of normal (16HBE14o−), but not CF (CFBE41o−, with ΔF508 CFTR mutation) epithelial cells. Expression of iNOS in inflammatory cells suggests that the gene is normal in CF. Absence of iNOS from bronchial epithelium may be due to low expression of the gene resulting from abnormalities in the signalling system that normally causes induction, such as cytokine receptors, second messengers or transcription factors. The resulting deficiency of the nitric oxide defence system may be relevant to the susceptibility of CF patients to pulmonary bacterial colonization. © 1998 John Wiley & Sons, Ltd.</description><identifier>ISSN: 0022-3417</identifier><identifier>EISSN: 1096-9896</identifier><identifier>DOI: 10.1002/(SICI)1096-9896(199803)184:3<323::AID-PATH2>3.0.CO;2-2</identifier><identifier>PMID: 9614386</identifier><identifier>CODEN: JPTLAS</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Adult ; Biological and medical sciences ; Bronchi - enzymology ; Bronchi - immunology ; bronchial epithelium ; Cell Culture Techniques ; cystic fibrosis ; Cystic Fibrosis - enzymology ; Cystic Fibrosis - immunology ; Cytokines - immunology ; Epithelium - enzymology ; Female ; Gene Expression ; Humans ; Immunoenzyme Techniques ; In Situ Hybridization ; inducible nitric oxide synthase ; inflammation ; Male ; Medical sciences ; Middle Aged ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Pneumology ; Polymerase Chain Reaction ; Respiratory system : syndromes and miscellaneous diseases ; RNA, Messenger - genetics</subject><ispartof>The Journal of pathology, 1998-03, Vol.184 (3), p.323-331</ispartof><rights>Copyright © 1998 John Wiley & Sons, Ltd.</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4322-2b227b039636a93d19db7ad913c83ce9321552d0dfb1c2f366a76e9de8b110f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291096-9896%28199803%29184%3A3%3C323%3A%3AAID-PATH2%3E3.0.CO%3B2-2$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291096-9896%28199803%29184%3A3%3C323%3A%3AAID-PATH2%3E3.0.CO%3B2-2$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2165028$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9614386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meng, Qing-Hai</creatorcontrib><creatorcontrib>Springall, David R.</creatorcontrib><creatorcontrib>Bishop, Anne E.</creatorcontrib><creatorcontrib>Morgan, Kevin</creatorcontrib><creatorcontrib>Evans, Tom J.</creatorcontrib><creatorcontrib>Habib, Said</creatorcontrib><creatorcontrib>Gruenert, Dieter C.</creatorcontrib><creatorcontrib>Gyi, Khin M.</creatorcontrib><creatorcontrib>Hodson, Margaret E.</creatorcontrib><creatorcontrib>Yacoub, Magdi H.</creatorcontrib><creatorcontrib>Polak, Julia M.</creatorcontrib><title>Lack of inducible nitric oxide synthase in bronchial epithelium: a possible mechanism of susceptibility to infection in cystic fibrosis</title><title>The Journal of pathology</title><addtitle>J. Pathol</addtitle><description>Cystic fibrosis (CF) is an inherited disorder associated with severe inflammation and repeated bacterial infection and colonization in the lung. Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro‐inflammatory cytokines can stimulate the expression of inducible nitric oxide synthase (iNOS), an enzyme generating nitric oxide, which functions as an important mediator in host defence mechanisms. To understand better the poor resistance to infections in the CF lung, the expression of the iNOS gene was investigated in explanted lungs from patients with cystic fibrosis (n‐13), bronchiectasis (n‐3), emphysema (n‐14), and in normal lungs (n‐8). In addition, bronchial epithelial cell lines were examined to study iNOS gene expression in vitro. Strong immunoreactivity for iNOS was seen in inflammatory cells and bronchial epithelium in all the diseased lungs, except for bronchial epithelium in CF. Quantitative analysis showed a significant reduction in the area of epithelium immunostained in CF [CF 6·8±1·6 (%±SEM); emphysema 18·2±2·8; normal 9·6±0·8, P<0·01], regardless of steroid treatment. These results were supported by in situ hybridization of iNOS mRNA, which showed a pattern of gene expression in CF, emphysema, and normal lung which paralleled that of protein immunoreactivity. Stimulation with cytokines (IL‐1β, TNF‐α, and IFN‐γ) increased the expression of iNOS mRNA detected by reverse transcriptase‐polymerase chain reaction (RT‐PCR) in cultures of normal (16HBE14o−), but not CF (CFBE41o−, with ΔF508 CFTR mutation) epithelial cells. Expression of iNOS in inflammatory cells suggests that the gene is normal in CF. Absence of iNOS from bronchial epithelium may be due to low expression of the gene resulting from abnormalities in the signalling system that normally causes induction, such as cytokine receptors, second messengers or transcription factors. The resulting deficiency of the nitric oxide defence system may be relevant to the susceptibility of CF patients to pulmonary bacterial colonization. © 1998 John Wiley & Sons, Ltd.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Bronchi - enzymology</subject><subject>Bronchi - immunology</subject><subject>bronchial epithelium</subject><subject>Cell Culture Techniques</subject><subject>cystic fibrosis</subject><subject>Cystic Fibrosis - enzymology</subject><subject>Cystic Fibrosis - immunology</subject><subject>Cytokines - immunology</subject><subject>Epithelium - enzymology</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>In Situ Hybridization</subject><subject>inducible nitric oxide synthase</subject><subject>inflammation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Pneumology</subject><subject>Polymerase Chain Reaction</subject><subject>Respiratory system : syndromes and miscellaneous diseases</subject><subject>RNA, Messenger - genetics</subject><issn>0022-3417</issn><issn>1096-9896</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd1u0zAYhiMEGmVwCUg5QGg7SPFP4sQdmlQCbJUqOonADj85jqOa5Y_Y0ZYr2G3jLFVPQOLIkr_Xj1_78bxLjJYYIfLh7Psm3ZxjxFnAE87OMOcJouc4CVf0IyV0tVpvPgc36-yaXNIlWqa7CxKQZ97ieOS5t3AgEtAQxy-9V8b8QghxHkUn3glnOKQJW3iPWyHv_Lb0dVMMUueV8httey399kEXyjdjY_fCKDf3875t5F6LyledtntV6aFe-cLvWmOeTtZK7kWjTT0BzWCk6qzOdaXt6NvWIUolrW6bCSZHY90tpXZUo81r70UpKqPeHNZT78fXL1l6HWx3V5t0vQ1kSN1bSE5InCPKGWWC0wLzIo9FwTGVCZWKU4KjiBSoKHMsSUkZEzFTvFBJjjEqQ3rqvZ-5Xd_-HpSxUGvXs6pEo9rBQMw5xlEcu-DPOShdP9OrErpe16IfASOYDAFMhmD6bpi-G2ZD4AwBBWcIwBmCJ0NuA0G6AwLEgd8eGgx5rYoj9qDEzd8d5sJIUZW9aKQ2xxjBLEIkcbHbOXavKzX-Ve5_3f5Vbd5w5GAma2PVw5Es-jtgMY0juP12BZ_C8IZlNIOM_gHHdcpN</recordid><startdate>199803</startdate><enddate>199803</enddate><creator>Meng, Qing-Hai</creator><creator>Springall, David R.</creator><creator>Bishop, Anne E.</creator><creator>Morgan, Kevin</creator><creator>Evans, Tom J.</creator><creator>Habib, Said</creator><creator>Gruenert, Dieter C.</creator><creator>Gyi, Khin M.</creator><creator>Hodson, Margaret E.</creator><creator>Yacoub, Magdi H.</creator><creator>Polak, Julia M.</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</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>7X8</scope></search><sort><creationdate>199803</creationdate><title>Lack of inducible nitric oxide synthase in bronchial epithelium: a possible mechanism of susceptibility to infection in cystic fibrosis</title><author>Meng, Qing-Hai ; Springall, David R. ; Bishop, Anne E. ; Morgan, Kevin ; Evans, Tom J. ; Habib, Said ; Gruenert, Dieter C. ; Gyi, Khin M. ; Hodson, Margaret E. ; Yacoub, Magdi H. ; Polak, Julia M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4322-2b227b039636a93d19db7ad913c83ce9321552d0dfb1c2f366a76e9de8b110f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Bronchi - enzymology</topic><topic>Bronchi - immunology</topic><topic>bronchial epithelium</topic><topic>Cell Culture Techniques</topic><topic>cystic fibrosis</topic><topic>Cystic Fibrosis - enzymology</topic><topic>Cystic Fibrosis - immunology</topic><topic>Cytokines - immunology</topic><topic>Epithelium - enzymology</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>In Situ Hybridization</topic><topic>inducible nitric oxide synthase</topic><topic>inflammation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Pneumology</topic><topic>Polymerase Chain Reaction</topic><topic>Respiratory system : syndromes and miscellaneous diseases</topic><topic>RNA, Messenger - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meng, Qing-Hai</creatorcontrib><creatorcontrib>Springall, David R.</creatorcontrib><creatorcontrib>Bishop, Anne E.</creatorcontrib><creatorcontrib>Morgan, Kevin</creatorcontrib><creatorcontrib>Evans, Tom J.</creatorcontrib><creatorcontrib>Habib, Said</creatorcontrib><creatorcontrib>Gruenert, Dieter C.</creatorcontrib><creatorcontrib>Gyi, Khin M.</creatorcontrib><creatorcontrib>Hodson, Margaret E.</creatorcontrib><creatorcontrib>Yacoub, Magdi H.</creatorcontrib><creatorcontrib>Polak, Julia M.</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>MEDLINE - Academic</collection><jtitle>The Journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meng, Qing-Hai</au><au>Springall, David R.</au><au>Bishop, Anne E.</au><au>Morgan, Kevin</au><au>Evans, Tom J.</au><au>Habib, Said</au><au>Gruenert, Dieter C.</au><au>Gyi, Khin M.</au><au>Hodson, Margaret E.</au><au>Yacoub, Magdi H.</au><au>Polak, Julia M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of inducible nitric oxide synthase in bronchial epithelium: a possible mechanism of susceptibility to infection in cystic fibrosis</atitle><jtitle>The Journal of pathology</jtitle><addtitle>J. Pathol</addtitle><date>1998-03</date><risdate>1998</risdate><volume>184</volume><issue>3</issue><spage>323</spage><epage>331</epage><pages>323-331</pages><issn>0022-3417</issn><eissn>1096-9896</eissn><coden>JPTLAS</coden><abstract>Cystic fibrosis (CF) is an inherited disorder associated with severe inflammation and repeated bacterial infection and colonization in the lung. Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro‐inflammatory cytokines can stimulate the expression of inducible nitric oxide synthase (iNOS), an enzyme generating nitric oxide, which functions as an important mediator in host defence mechanisms. To understand better the poor resistance to infections in the CF lung, the expression of the iNOS gene was investigated in explanted lungs from patients with cystic fibrosis (n‐13), bronchiectasis (n‐3), emphysema (n‐14), and in normal lungs (n‐8). In addition, bronchial epithelial cell lines were examined to study iNOS gene expression in vitro. Strong immunoreactivity for iNOS was seen in inflammatory cells and bronchial epithelium in all the diseased lungs, except for bronchial epithelium in CF. Quantitative analysis showed a significant reduction in the area of epithelium immunostained in CF [CF 6·8±1·6 (%±SEM); emphysema 18·2±2·8; normal 9·6±0·8, P<0·01], regardless of steroid treatment. These results were supported by in situ hybridization of iNOS mRNA, which showed a pattern of gene expression in CF, emphysema, and normal lung which paralleled that of protein immunoreactivity. Stimulation with cytokines (IL‐1β, TNF‐α, and IFN‐γ) increased the expression of iNOS mRNA detected by reverse transcriptase‐polymerase chain reaction (RT‐PCR) in cultures of normal (16HBE14o−), but not CF (CFBE41o−, with ΔF508 CFTR mutation) epithelial cells. Expression of iNOS in inflammatory cells suggests that the gene is normal in CF. Absence of iNOS from bronchial epithelium may be due to low expression of the gene resulting from abnormalities in the signalling system that normally causes induction, such as cytokine receptors, second messengers or transcription factors. The resulting deficiency of the nitric oxide defence system may be relevant to the susceptibility of CF patients to pulmonary bacterial colonization. © 1998 John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>9614386</pmid><doi>10.1002/(SICI)1096-9896(199803)184:3<323::AID-PATH2>3.0.CO;2-2</doi><tpages>9</tpages></addata></record> |
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| subjects | Adult Biological and medical sciences Bronchi - enzymology Bronchi - immunology bronchial epithelium Cell Culture Techniques cystic fibrosis Cystic Fibrosis - enzymology Cystic Fibrosis - immunology Cytokines - immunology Epithelium - enzymology Female Gene Expression Humans Immunoenzyme Techniques In Situ Hybridization inducible nitric oxide synthase inflammation Male Medical sciences Middle Aged Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Pneumology Polymerase Chain Reaction Respiratory system : syndromes and miscellaneous diseases RNA, Messenger - genetics |
| title | Lack of inducible nitric oxide synthase in bronchial epithelium: a possible mechanism of susceptibility to infection in cystic fibrosis |
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