Transcriptional response of bronchial epithelial cells to Pseudomonas aeruginosa: identification of early mediators of host defense
1 Department of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands 2 Department of Dermatology, University Medical Center St. Radboud, Nijmegen, The Netherlands 3 Department of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Leiden University Medical Center, Leid...
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| Veröffentlicht in: | Physiological genomics 2005-05, Vol.21 (3), p.324-336 |
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| creator | Vos, Joost B van Sterkenburg, Marianne A Rabe, Klaus F Schalkwijk, Joost Hiemstra, Pieter S Datson, Nicole A |
| description | 1 Department of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands
2 Department of Dermatology, University Medical Center St. Radboud, Nijmegen, The Netherlands
3 Department of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Leiden University Medical Center, Leiden, The Netherlands
The airway epithelium responds to microbial exposure by altering expression of a variety of genes to increase innate host defense. We aimed to delineate the early transcriptional response in human primary bronchial epithelial cells exposed for 6 h to a mixture of IL-1ß and TNF- or heat-inactivated Pseudomonas aeruginosa. Because molecular mechanisms of epithelial innate host defense are not fully understood, the open-ended expression-profiling technique SAGE was applied to construct gene expression profiles covering 30,000 genes: 292 genes were found to be differentially expressed. Expression of seven genes was confirmed by real-time qPCR. Among differentially expressed genes, four classes or families were identified: keratins, proteinase inhibitors, S100 calcium-binding proteins, and IL-1 family members. Marked transcriptional changes were observed for keratins that form a key component of the cytoskeleton in epithelial cells. Expression of antimicrobial proteinase inhibitors SLPI and elafin was elevated after microbial or cytokine exposure. Interestingly, expression of numerous S100 family members was observed, and eight members, including S100A8 and S100A9, were among the most differentially expressed genes. Differential expression was also observed for the IL-1 family members IL-1ß, IL-1 receptor antagonist, and IL-1F9, a newly discovered IL-1 family member. Clustering of differentially expressed genes into biological processes revealed that the early inflammatory response in airway epithelial cells to IL-1ß-TNF- and P. aeruginosa is characterized by expression of genes involved in epithelial barrier formation and host defense.
serial analysis of gene expression; primary bronchial epithelial cells; airway inflammation; innate immunity; secretory leukocyte proteinase inhibitor |
| doi_str_mv | 10.1152/physiolgenomics.00289.2004 |
| format | Article |
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2 Department of Dermatology, University Medical Center St. Radboud, Nijmegen, The Netherlands
3 Department of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Leiden University Medical Center, Leiden, The Netherlands
The airway epithelium responds to microbial exposure by altering expression of a variety of genes to increase innate host defense. We aimed to delineate the early transcriptional response in human primary bronchial epithelial cells exposed for 6 h to a mixture of IL-1ß and TNF- or heat-inactivated Pseudomonas aeruginosa. Because molecular mechanisms of epithelial innate host defense are not fully understood, the open-ended expression-profiling technique SAGE was applied to construct gene expression profiles covering 30,000 genes: 292 genes were found to be differentially expressed. Expression of seven genes was confirmed by real-time qPCR. Among differentially expressed genes, four classes or families were identified: keratins, proteinase inhibitors, S100 calcium-binding proteins, and IL-1 family members. Marked transcriptional changes were observed for keratins that form a key component of the cytoskeleton in epithelial cells. Expression of antimicrobial proteinase inhibitors SLPI and elafin was elevated after microbial or cytokine exposure. Interestingly, expression of numerous S100 family members was observed, and eight members, including S100A8 and S100A9, were among the most differentially expressed genes. Differential expression was also observed for the IL-1 family members IL-1ß, IL-1 receptor antagonist, and IL-1F9, a newly discovered IL-1 family member. Clustering of differentially expressed genes into biological processes revealed that the early inflammatory response in airway epithelial cells to IL-1ß-TNF- and P. aeruginosa is characterized by expression of genes involved in epithelial barrier formation and host defense.
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2 Department of Dermatology, University Medical Center St. Radboud, Nijmegen, The Netherlands
3 Department of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Leiden University Medical Center, Leiden, The Netherlands
The airway epithelium responds to microbial exposure by altering expression of a variety of genes to increase innate host defense. We aimed to delineate the early transcriptional response in human primary bronchial epithelial cells exposed for 6 h to a mixture of IL-1ß and TNF- or heat-inactivated Pseudomonas aeruginosa. Because molecular mechanisms of epithelial innate host defense are not fully understood, the open-ended expression-profiling technique SAGE was applied to construct gene expression profiles covering 30,000 genes: 292 genes were found to be differentially expressed. Expression of seven genes was confirmed by real-time qPCR. Among differentially expressed genes, four classes or families were identified: keratins, proteinase inhibitors, S100 calcium-binding proteins, and IL-1 family members. Marked transcriptional changes were observed for keratins that form a key component of the cytoskeleton in epithelial cells. Expression of antimicrobial proteinase inhibitors SLPI and elafin was elevated after microbial or cytokine exposure. Interestingly, expression of numerous S100 family members was observed, and eight members, including S100A8 and S100A9, were among the most differentially expressed genes. Differential expression was also observed for the IL-1 family members IL-1ß, IL-1 receptor antagonist, and IL-1F9, a newly discovered IL-1 family member. Clustering of differentially expressed genes into biological processes revealed that the early inflammatory response in airway epithelial cells to IL-1ß-TNF- and P. aeruginosa is characterized by expression of genes involved in epithelial barrier formation and host defense.
serial analysis of gene expression; primary bronchial epithelial cells; airway inflammation; innate immunity; secretory leukocyte proteinase inhibitor</description><subject>Bronchi</subject><subject>Cell Culture Techniques - methods</subject><subject>Cells, Cultured</subject><subject>Databases, Nucleic Acid</subject><subject>DNA Primers</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin-1 - genetics</subject><subject>Interleukin-1 - pharmacology</subject><subject>Polymerase Chain Reaction</subject><subject>Pseudomonas aeruginosa</subject><subject>Respiratory Mucosa - cytology</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - microbiology</subject><subject>Respiratory Mucosa - physiology</subject><subject>RNA - genetics</subject><subject>RNA - isolation & purification</subject><subject>Transcription, Genetic</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>1094-8341</issn><issn>1531-2267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV-L1DAUxYso7rr6FST44FvH_GmazL6ILK4KC_owPoc0vZ1G0qbmtug8-8U33ZlFGBDzkFwu5_xuklMUbxjdMCb5u6k_oI9hD2McvMMNpVxvN5zS6klxyaRgJee1eppruq1KLSp2UbxA_EEpq5SWz4sLJhVlim8viz-7ZEd0yU-zj6MNJAFOcUQgsSNNiqPrfe7C5Ocewlo6CAHJHMk3hKWNQ3YhsZCWvR8j2mviWxhn33lnV-TKAZvCgQzQejvHhGurjziTFjrIo14WzzobEF6dzqvi--3H3c3n8u7rpy83H-5KJ1k1l4o1oGyjlJWNo5LbmmkqtFA1rajSrmu0ZlspuWBN3jrngEsunaKqycuJq-LtkTul-HMBnM3gcX2OHSEuaGqluawp_a-QU61rKassvD4KXYqICTozJT_YdDCMmjUrc5aVecjKrFll8-vTlKXJf_PXegonC94fBb3f9798gkda3B_M7RLCDn7P5xM4M8IIXpmp7TJB_JtwfrVHp7gHX0vDvw</recordid><startdate>20050511</startdate><enddate>20050511</enddate><creator>Vos, Joost B</creator><creator>van Sterkenburg, Marianne A</creator><creator>Rabe, Klaus F</creator><creator>Schalkwijk, Joost</creator><creator>Hiemstra, Pieter S</creator><creator>Datson, Nicole A</creator><general>Am Physiological Soc</general><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>7QL</scope><scope>7TM</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050511</creationdate><title>Transcriptional response of bronchial epithelial cells to Pseudomonas aeruginosa: identification of early mediators of host defense</title><author>Vos, Joost B ; van Sterkenburg, Marianne A ; Rabe, Klaus F ; Schalkwijk, Joost ; Hiemstra, Pieter S ; Datson, Nicole A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-71be7ab77a5bc052a61803837604078cfb881955231b523fcce2525c707bbbbc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Bronchi</topic><topic>Cell Culture Techniques - methods</topic><topic>Cells, Cultured</topic><topic>Databases, Nucleic Acid</topic><topic>DNA Primers</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin-1 - genetics</topic><topic>Interleukin-1 - pharmacology</topic><topic>Polymerase Chain Reaction</topic><topic>Pseudomonas aeruginosa</topic><topic>Respiratory Mucosa - cytology</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - microbiology</topic><topic>Respiratory Mucosa - physiology</topic><topic>RNA - genetics</topic><topic>RNA - isolation & purification</topic><topic>Transcription, Genetic</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vos, Joost B</creatorcontrib><creatorcontrib>van Sterkenburg, Marianne A</creatorcontrib><creatorcontrib>Rabe, Klaus F</creatorcontrib><creatorcontrib>Schalkwijk, Joost</creatorcontrib><creatorcontrib>Hiemstra, Pieter S</creatorcontrib><creatorcontrib>Datson, Nicole A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Physiological genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vos, Joost B</au><au>van Sterkenburg, Marianne A</au><au>Rabe, Klaus F</au><au>Schalkwijk, Joost</au><au>Hiemstra, Pieter S</au><au>Datson, Nicole A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcriptional response of bronchial epithelial cells to Pseudomonas aeruginosa: identification of early mediators of host defense</atitle><jtitle>Physiological genomics</jtitle><addtitle>Physiol Genomics</addtitle><date>2005-05-11</date><risdate>2005</risdate><volume>21</volume><issue>3</issue><spage>324</spage><epage>336</epage><pages>324-336</pages><issn>1094-8341</issn><eissn>1531-2267</eissn><abstract>1 Department of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands
2 Department of Dermatology, University Medical Center St. Radboud, Nijmegen, The Netherlands
3 Department of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Leiden University Medical Center, Leiden, The Netherlands
The airway epithelium responds to microbial exposure by altering expression of a variety of genes to increase innate host defense. We aimed to delineate the early transcriptional response in human primary bronchial epithelial cells exposed for 6 h to a mixture of IL-1ß and TNF- or heat-inactivated Pseudomonas aeruginosa. Because molecular mechanisms of epithelial innate host defense are not fully understood, the open-ended expression-profiling technique SAGE was applied to construct gene expression profiles covering 30,000 genes: 292 genes were found to be differentially expressed. Expression of seven genes was confirmed by real-time qPCR. Among differentially expressed genes, four classes or families were identified: keratins, proteinase inhibitors, S100 calcium-binding proteins, and IL-1 family members. Marked transcriptional changes were observed for keratins that form a key component of the cytoskeleton in epithelial cells. Expression of antimicrobial proteinase inhibitors SLPI and elafin was elevated after microbial or cytokine exposure. Interestingly, expression of numerous S100 family members was observed, and eight members, including S100A8 and S100A9, were among the most differentially expressed genes. Differential expression was also observed for the IL-1 family members IL-1ß, IL-1 receptor antagonist, and IL-1F9, a newly discovered IL-1 family member. Clustering of differentially expressed genes into biological processes revealed that the early inflammatory response in airway epithelial cells to IL-1ß-TNF- and P. aeruginosa is characterized by expression of genes involved in epithelial barrier formation and host defense.
serial analysis of gene expression; primary bronchial epithelial cells; airway inflammation; innate immunity; secretory leukocyte proteinase inhibitor</abstract><cop>United States</cop><pub>Am Physiological Soc</pub><pmid>15701729</pmid><doi>10.1152/physiolgenomics.00289.2004</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1094-8341 |
| ispartof | Physiological genomics, 2005-05, Vol.21 (3), p.324-336 |
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| language | eng |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Bronchi Cell Culture Techniques - methods Cells, Cultured Databases, Nucleic Acid DNA Primers Gene Expression Regulation Humans Inflammation Interleukin-1 - genetics Interleukin-1 - pharmacology Polymerase Chain Reaction Pseudomonas aeruginosa Respiratory Mucosa - cytology Respiratory Mucosa - drug effects Respiratory Mucosa - microbiology Respiratory Mucosa - physiology RNA - genetics RNA - isolation & purification Transcription, Genetic Tumor Necrosis Factor-alpha - pharmacology |
| title | Transcriptional response of bronchial epithelial cells to Pseudomonas aeruginosa: identification of early mediators of host defense |
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