TLR-4-mediated innate immunity is reduced in cystic fibrosis airway cells
Airway epithelial cells contribute to the inflammatory response of the lung, and their innate immune response is primarily mediated via Toll-like receptor (TLR) signaling. Cystic fibrosis (CF) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified immune response in CF....
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2010-04, Vol.42 (4), p.424-431 |
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| creator | John, Gerrit Yildirim, Ali O Rubin, Bruce K Gruenert, Dieter C Henke, Markus O |
| description | Airway epithelial cells contribute to the inflammatory response of the lung, and their innate immune response is primarily mediated via Toll-like receptor (TLR) signaling. Cystic fibrosis (CF) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified immune response in CF. We investigated the TLR-4 expression and the inflammatory profile (IL-8 and IL-6 secretion) in CF bronchial epithelial cell line CFBE41o- and its CF transmembrane ion condcutance regulator (CFTR)-corrected counterpart grown under air-liquid interface conditions after stimulation with lipopolysaccharide (LPS) from gram-negative bacteria. In CFTR-corrected cells, IL-8 and IL-6 secretions were constitutively activated but significantly increased after LPS stimulation compared with CFBE41o-. Blocking TLR-4 by a specific antibody significantly inhibited IL-8 secretion only in CFTR-corrected cells. Transfection with specific siRNA directed against TLR-4 mRNA significantly reduced the response to LPS in both cell lines. Fluorescence-activated cell sorter analysis revealed significantly higher levels of TLR-4 surface expression in CFTR-corrected cells. In histologic lung sections of patients with CF, the TLR-4 expression in the bronchial epithelium was significantly reduced compared with healthy control subjects. In CF the loss of CFTR function appears to decrease innate immune responses, possibly by altering the expression of TLR-4 on airway epithelial cells. This may contribute to chronic bacterial infection of CF airways. |
| doi_str_mv | 10.1165/rcmb.2008-0408OC |
| format | Article |
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Cystic fibrosis (CF) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified immune response in CF. We investigated the TLR-4 expression and the inflammatory profile (IL-8 and IL-6 secretion) in CF bronchial epithelial cell line CFBE41o- and its CF transmembrane ion condcutance regulator (CFTR)-corrected counterpart grown under air-liquid interface conditions after stimulation with lipopolysaccharide (LPS) from gram-negative bacteria. In CFTR-corrected cells, IL-8 and IL-6 secretions were constitutively activated but significantly increased after LPS stimulation compared with CFBE41o-. Blocking TLR-4 by a specific antibody significantly inhibited IL-8 secretion only in CFTR-corrected cells. Transfection with specific siRNA directed against TLR-4 mRNA significantly reduced the response to LPS in both cell lines. Fluorescence-activated cell sorter analysis revealed significantly higher levels of TLR-4 surface expression in CFTR-corrected cells. In histologic lung sections of patients with CF, the TLR-4 expression in the bronchial epithelium was significantly reduced compared with healthy control subjects. In CF the loss of CFTR function appears to decrease innate immune responses, possibly by altering the expression of TLR-4 on airway epithelial cells. This may contribute to chronic bacterial infection of CF airways.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2008-0408OC</identifier><identifier>PMID: 19502387</identifier><identifier>CODEN: AJRBEL</identifier><language>eng</language><publisher>United States: American Thoracic Society</publisher><subject>Adolescent ; Adult ; Antibodies - immunology ; Antibodies - pharmacology ; Bronchi - immunology ; Bronchi - metabolism ; Bronchi - pathology ; Cell Line ; Child ; Cystic Fibrosis - genetics ; Cystic Fibrosis - immunology ; Cystic Fibrosis - metabolism ; Cystic Fibrosis - pathology ; Cystic Fibrosis Transmembrane Conductance Regulator - genetics ; Cystic Fibrosis Transmembrane Conductance Regulator - immunology ; Cystic Fibrosis Transmembrane Conductance Regulator - metabolism ; Epithelial Cells - immunology ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Female ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - genetics ; Gene Expression Regulation - immunology ; Humans ; Immunity, Innate ; Interleukin-6 - biosynthesis ; Interleukin-6 - immunology ; Interleukin-8 - biosynthesis ; Interleukin-8 - immunology ; Lipopolysaccharides - pharmacology ; Male ; Pseudomonas aeruginosa - immunology ; Pseudomonas Infections - genetics ; Pseudomonas Infections - immunology ; Pseudomonas Infections - metabolism ; Pseudomonas Infections - pathology ; Respiratory Mucosa - immunology ; Respiratory Mucosa - metabolism ; Respiratory Mucosa - pathology ; RNA, Messenger - biosynthesis ; RNA, Messenger - immunology ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Signal Transduction - immunology ; Toll-Like Receptor 4 - antagonists & inhibitors ; Toll-Like Receptor 4 - biosynthesis ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - immunology</subject><ispartof>American journal of respiratory cell and molecular biology, 2010-04, Vol.42 (4), p.424-431</ispartof><rights>Copyright American Thoracic Society Apr 2010</rights><rights>2010 The American Thoracic Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-69219a04f6abfc8e75ce595e1c4c5540aceccf26593ce5e94a89d347758c085e3</citedby><cites>FETCH-LOGICAL-c469t-69219a04f6abfc8e75ce595e1c4c5540aceccf26593ce5e94a89d347758c085e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19502387$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>John, Gerrit</creatorcontrib><creatorcontrib>Yildirim, Ali O</creatorcontrib><creatorcontrib>Rubin, Bruce K</creatorcontrib><creatorcontrib>Gruenert, Dieter C</creatorcontrib><creatorcontrib>Henke, Markus O</creatorcontrib><title>TLR-4-mediated innate immunity is reduced in cystic fibrosis airway cells</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>Airway epithelial cells contribute to the inflammatory response of the lung, and their innate immune response is primarily mediated via Toll-like receptor (TLR) signaling. Cystic fibrosis (CF) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified immune response in CF. We investigated the TLR-4 expression and the inflammatory profile (IL-8 and IL-6 secretion) in CF bronchial epithelial cell line CFBE41o- and its CF transmembrane ion condcutance regulator (CFTR)-corrected counterpart grown under air-liquid interface conditions after stimulation with lipopolysaccharide (LPS) from gram-negative bacteria. In CFTR-corrected cells, IL-8 and IL-6 secretions were constitutively activated but significantly increased after LPS stimulation compared with CFBE41o-. Blocking TLR-4 by a specific antibody significantly inhibited IL-8 secretion only in CFTR-corrected cells. Transfection with specific siRNA directed against TLR-4 mRNA significantly reduced the response to LPS in both cell lines. Fluorescence-activated cell sorter analysis revealed significantly higher levels of TLR-4 surface expression in CFTR-corrected cells. In histologic lung sections of patients with CF, the TLR-4 expression in the bronchial epithelium was significantly reduced compared with healthy control subjects. In CF the loss of CFTR function appears to decrease innate immune responses, possibly by altering the expression of TLR-4 on airway epithelial cells. This may contribute to chronic bacterial infection of CF airways.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Antibodies - immunology</subject><subject>Antibodies - pharmacology</subject><subject>Bronchi - immunology</subject><subject>Bronchi - metabolism</subject><subject>Bronchi - pathology</subject><subject>Cell Line</subject><subject>Child</subject><subject>Cystic Fibrosis - genetics</subject><subject>Cystic Fibrosis - immunology</subject><subject>Cystic Fibrosis - metabolism</subject><subject>Cystic Fibrosis - pathology</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - genetics</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - immunology</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - metabolism</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Female</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene Expression Regulation - immunology</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Interleukin-6 - immunology</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Interleukin-8 - immunology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Pseudomonas aeruginosa - immunology</subject><subject>Pseudomonas Infections - genetics</subject><subject>Pseudomonas Infections - immunology</subject><subject>Pseudomonas Infections - metabolism</subject><subject>Pseudomonas Infections - pathology</subject><subject>Respiratory Mucosa - immunology</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Respiratory Mucosa - pathology</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - immunology</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><subject>Toll-Like Receptor 4 - antagonists & inhibitors</subject><subject>Toll-Like Receptor 4 - biosynthesis</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - immunology</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpVkN1LwzAUxYMobk7ffZLie2bSJG3yIsjwYzAYyHwO6W2qGWs7k1bpf2_mhh8QuIFz77nn_hC6pGRKaSZuPNTFNCVEYsKJXM6O0JgKJjBXUh3HP-EcU8HVCJ2FsCaEppLSUzSiSpCUyXyM5qvFM-a4tqUznS0T1zSxJq6u-8Z1Q-JC4m3Zw7eUwBA6B0nlCt-GKBnnP82QgN1swjk6qcwm2ItDnaCXh_vV7Akvlo_z2d0CA89UhzOVUmUIrzJTVCBtLsAKJSwFDkJwYsACVGkmFIuCVdxIVTKe50ICkcKyCbrd-277IsYG23TebPTWu9r4QbfG6f9K4970a_uhBY97GIkG1wcD3773NnR63fa-iZl1SvKMZfHFJrJvgnhp8Lb6WUCJ3rHXO_Z6x17v2ceRq7_BfgcOsNkXznuBiw</recordid><startdate>201004</startdate><enddate>201004</enddate><creator>John, Gerrit</creator><creator>Yildirim, Ali O</creator><creator>Rubin, Bruce K</creator><creator>Gruenert, Dieter C</creator><creator>Henke, Markus O</creator><general>American Thoracic Society</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>5PM</scope></search><sort><creationdate>201004</creationdate><title>TLR-4-mediated innate immunity is reduced in cystic fibrosis airway cells</title><author>John, Gerrit ; Yildirim, Ali O ; Rubin, Bruce K ; Gruenert, Dieter C ; Henke, Markus O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-69219a04f6abfc8e75ce595e1c4c5540aceccf26593ce5e94a89d347758c085e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Antibodies - 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immunology</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Interleukin-8 - immunology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Pseudomonas aeruginosa - immunology</topic><topic>Pseudomonas Infections - genetics</topic><topic>Pseudomonas Infections - immunology</topic><topic>Pseudomonas Infections - metabolism</topic><topic>Pseudomonas Infections - pathology</topic><topic>Respiratory Mucosa - immunology</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Respiratory Mucosa - pathology</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - immunology</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - immunology</topic><topic>Toll-Like Receptor 4 - antagonists & inhibitors</topic><topic>Toll-Like Receptor 4 - biosynthesis</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>John, Gerrit</creatorcontrib><creatorcontrib>Yildirim, Ali O</creatorcontrib><creatorcontrib>Rubin, Bruce K</creatorcontrib><creatorcontrib>Gruenert, Dieter C</creatorcontrib><creatorcontrib>Henke, Markus O</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>John, Gerrit</au><au>Yildirim, Ali O</au><au>Rubin, Bruce K</au><au>Gruenert, Dieter C</au><au>Henke, Markus O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR-4-mediated innate immunity is reduced in cystic fibrosis airway cells</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2010-04</date><risdate>2010</risdate><volume>42</volume><issue>4</issue><spage>424</spage><epage>431</epage><pages>424-431</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><coden>AJRBEL</coden><abstract>Airway epithelial cells contribute to the inflammatory response of the lung, and their innate immune response is primarily mediated via Toll-like receptor (TLR) signaling. Cystic fibrosis (CF) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified immune response in CF. We investigated the TLR-4 expression and the inflammatory profile (IL-8 and IL-6 secretion) in CF bronchial epithelial cell line CFBE41o- and its CF transmembrane ion condcutance regulator (CFTR)-corrected counterpart grown under air-liquid interface conditions after stimulation with lipopolysaccharide (LPS) from gram-negative bacteria. In CFTR-corrected cells, IL-8 and IL-6 secretions were constitutively activated but significantly increased after LPS stimulation compared with CFBE41o-. Blocking TLR-4 by a specific antibody significantly inhibited IL-8 secretion only in CFTR-corrected cells. Transfection with specific siRNA directed against TLR-4 mRNA significantly reduced the response to LPS in both cell lines. Fluorescence-activated cell sorter analysis revealed significantly higher levels of TLR-4 surface expression in CFTR-corrected cells. In histologic lung sections of patients with CF, the TLR-4 expression in the bronchial epithelium was significantly reduced compared with healthy control subjects. In CF the loss of CFTR function appears to decrease innate immune responses, possibly by altering the expression of TLR-4 on airway epithelial cells. This may contribute to chronic bacterial infection of CF airways.</abstract><cop>United States</cop><pub>American Thoracic Society</pub><pmid>19502387</pmid><doi>10.1165/rcmb.2008-0408OC</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of respiratory cell and molecular biology, 2010-04, Vol.42 (4), p.424-431 |
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| source | MEDLINE; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adolescent Adult Antibodies - immunology Antibodies - pharmacology Bronchi - immunology Bronchi - metabolism Bronchi - pathology Cell Line Child Cystic Fibrosis - genetics Cystic Fibrosis - immunology Cystic Fibrosis - metabolism Cystic Fibrosis - pathology Cystic Fibrosis Transmembrane Conductance Regulator - genetics Cystic Fibrosis Transmembrane Conductance Regulator - immunology Cystic Fibrosis Transmembrane Conductance Regulator - metabolism Epithelial Cells - immunology Epithelial Cells - metabolism Epithelial Cells - pathology Female Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Gene Expression Regulation - immunology Humans Immunity, Innate Interleukin-6 - biosynthesis Interleukin-6 - immunology Interleukin-8 - biosynthesis Interleukin-8 - immunology Lipopolysaccharides - pharmacology Male Pseudomonas aeruginosa - immunology Pseudomonas Infections - genetics Pseudomonas Infections - immunology Pseudomonas Infections - metabolism Pseudomonas Infections - pathology Respiratory Mucosa - immunology Respiratory Mucosa - metabolism Respiratory Mucosa - pathology RNA, Messenger - biosynthesis RNA, Messenger - immunology Signal Transduction - drug effects Signal Transduction - genetics Signal Transduction - immunology Toll-Like Receptor 4 - antagonists & inhibitors Toll-Like Receptor 4 - biosynthesis Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - immunology |
| title | TLR-4-mediated innate immunity is reduced in cystic fibrosis airway cells |
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