CpG DNA-mediated immune response in pulmonary endothelial cells.
Identifieur interne : 001F15 ( Main/Exploration ); précédent : 001F14; suivant : 001F16CpG DNA-mediated immune response in pulmonary endothelial cells.
Auteurs : Jiang Li [États-Unis] ; Zheng Ma ; Zhi-Lue Tang ; Troy Stevens ; Bruce Pitt ; Song LiSource :
- American journal of physiology. Lung cellular and molecular physiology [ 1040-0605 ] ; 2004.
Descripteurs français
- KwdFr :
- ADN bactérien (immunologie), ADN bactérien (pharmacologie), ARN messager (métabolisme), Animaux, Antipaludiques (pharmacologie), Chloroquine (pharmacologie), Escherichia coli (génétique), Expression des gènes (), Expression des gènes (immunologie), Ilots CpG (immunologie), Interleukine-8 (génétique), Lipopolysaccharides (pharmacologie), Molécule-1 d'adhérence intercellulaire (génétique), Muqueuse respiratoire (cytologie), Muqueuse respiratoire (immunologie), Oligonucléotides (immunologie), Oligonucléotides (pharmacologie), Plasmides (immunologie), Protéines de liaison à l'ADN (génétique), Rats, Récepteur-9 de type Toll-like, Récepteurs de surface cellulaire (génétique), Régulation positive (immunologie), Souris, Synergie des médicaments, Techniques de transfert de gènes, Transduction du signal (immunologie).
- MESH :
- cytologie : Muqueuse respiratoire.
- génétique : Escherichia coli, Interleukine-8, Molécule-1 d'adhérence intercellulaire, Protéines de liaison à l'ADN, Récepteurs de surface cellulaire.
- immunologie : ADN bactérien, Expression des gènes, Ilots CpG, Muqueuse respiratoire, Oligonucléotides, Plasmides, Régulation positive, Transduction du signal.
- métabolisme : ARN messager.
- pharmacologie : ADN bactérien, Antipaludiques, Chloroquine, Lipopolysaccharides, Oligonucléotides.
- Animaux, Expression des gènes, Rats, Récepteur-9 de type Toll-like, Souris, Synergie des médicaments, Techniques de transfert de gènes.
English descriptors
- KwdEn :
- Animals, Antimalarials (pharmacology), Chloroquine (pharmacology), CpG Islands (immunology), DNA, Bacterial (immunology), DNA, Bacterial (pharmacology), DNA-Binding Proteins (genetics), Drug Synergism, Escherichia coli (genetics), Gene Expression (drug effects), Gene Expression (immunology), Gene Transfer Techniques, Intercellular Adhesion Molecule-1 (genetics), Interleukin-8 (genetics), Lipopolysaccharides (pharmacology), Mice, Oligonucleotides (immunology), Oligonucleotides (pharmacology), Plasmids (immunology), RNA, Messenger (metabolism), Rats, Receptors, Cell Surface (genetics), Respiratory Mucosa (cytology), Respiratory Mucosa (immunology), Signal Transduction (immunology), Toll-Like Receptor 9, Up-Regulation (immunology).
- MESH :
- chemical , genetics : DNA-Binding Proteins, Intercellular Adhesion Molecule-1, Interleukin-8, Receptors, Cell Surface.
- chemical , immunology : DNA, Bacterial, Oligonucleotides.
- chemical , metabolism : RNA, Messenger.
- chemical , pharmacology : Antimalarials, Chloroquine, DNA, Bacterial, Lipopolysaccharides, Oligonucleotides.
- cytology : Respiratory Mucosa.
- drug effects : Gene Expression.
- genetics : Escherichia coli.
- immunology : CpG Islands, Gene Expression, Plasmids, Respiratory Mucosa, Signal Transduction, Up-Regulation.
- Animals, Drug Synergism, Gene Transfer Techniques, Mice, Rats, Toll-Like Receptor 9.
Abstract
Although the CpG DNA immune response mediated by Toll-like receptor 9 (TLR9) has been extensively studied in a number of immune cells, the response to CpG DNA in endothelial cells (EC) is not well understood. In this study, we show that both mouse and rat lung EC display constitutive expression of TLR9 mRNA. Exposure to CpG DNA induced a potent proinflammatory response as manifested by an increased expression of IL-8 and ICAM-1 in mouse pulmonary EC. The proinflammatory response was sensitive to chloroquine, consistent with a role of endosomal contribution. A role for p38 MAPK and NF-kappaB pathway was apparent as the response was sensitive to inhibitors of p38 MAPK and NF-kappaB but was not affected by inhibitors of ERK1/2. A synergistic effect of CpG DNA and LPS on the inflammatory response is consistent with multiple TLR interaction in EC. This study suggests a possible role for CpG DNA-mediated EC immune response in the host defense system. It also has important implications in plasmid DNA-mediated pulmonary endothelium gene transfer.
DOI: 10.1152/ajplung.00436.2003
PubMed: 15155271
Affiliations:
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Le document en format XML
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Lung cellular and molecular physiology</title><idno type="ISSN">1040-0605</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antimalarials (pharmacology)</term><term>Chloroquine (pharmacology)</term><term>CpG Islands (immunology)</term><term>DNA, Bacterial (immunology)</term><term>DNA, Bacterial (pharmacology)</term><term>DNA-Binding Proteins (genetics)</term><term>Drug Synergism</term><term>Escherichia coli (genetics)</term><term>Gene Expression (drug effects)</term><term>Gene Expression (immunology)</term><term>Gene Transfer Techniques</term><term>Intercellular Adhesion Molecule-1 (genetics)</term><term>Interleukin-8 (genetics)</term><term>Lipopolysaccharides (pharmacology)</term><term>Mice</term><term>Oligonucleotides (immunology)</term><term>Oligonucleotides (pharmacology)</term><term>Plasmids (immunology)</term><term>RNA, Messenger (metabolism)</term><term>Rats</term><term>Receptors, Cell Surface (genetics)</term><term>Respiratory Mucosa (cytology)</term><term>Respiratory Mucosa (immunology)</term><term>Signal Transduction (immunology)</term><term>Toll-Like Receptor 9</term><term>Up-Regulation (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN bactérien (immunologie)</term><term>ADN bactérien (pharmacologie)</term><term>ARN messager (métabolisme)</term><term>Animaux</term><term>Antipaludiques (pharmacologie)</term><term>Chloroquine (pharmacologie)</term><term>Escherichia coli (génétique)</term><term>Expression des gènes ()</term><term>Expression des gènes (immunologie)</term><term>Ilots CpG (immunologie)</term><term>Interleukine-8 (génétique)</term><term>Lipopolysaccharides (pharmacologie)</term><term>Molécule-1 d'adhérence intercellulaire (génétique)</term><term>Muqueuse respiratoire (cytologie)</term><term>Muqueuse respiratoire (immunologie)</term><term>Oligonucléotides (immunologie)</term><term>Oligonucléotides (pharmacologie)</term><term>Plasmides (immunologie)</term><term>Protéines de liaison à l'ADN (génétique)</term><term>Rats</term><term>Récepteur-9 de type Toll-like</term><term>Récepteurs de surface cellulaire (génétique)</term><term>Régulation positive (immunologie)</term><term>Souris</term><term>Synergie des médicaments</term><term>Techniques de transfert de gènes</term><term>Transduction du signal (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA-Binding Proteins</term><term>Intercellular Adhesion Molecule-1</term><term>Interleukin-8</term><term>Receptors, Cell Surface</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>DNA, Bacterial</term><term>Oligonucleotides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antimalarials</term><term>Chloroquine</term><term>DNA, Bacterial</term><term>Lipopolysaccharides</term><term>Oligonucleotides</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Muqueuse respiratoire</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Escherichia coli</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Escherichia coli</term><term>Interleukine-8</term><term>Molécule-1 d'adhérence intercellulaire</term><term>Protéines de liaison à l'ADN</term><term>Récepteurs de surface cellulaire</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>ADN bactérien</term><term>Expression des gènes</term><term>Ilots CpG</term><term>Muqueuse respiratoire</term><term>Oligonucléotides</term><term>Plasmides</term><term>Régulation positive</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CpG Islands</term><term>Gene Expression</term><term>Plasmids</term><term>Respiratory Mucosa</term><term>Signal Transduction</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>ADN bactérien</term><term>Antipaludiques</term><term>Chloroquine</term><term>Lipopolysaccharides</term><term>Oligonucléotides</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Synergism</term><term>Gene Transfer Techniques</term><term>Mice</term><term>Rats</term><term>Toll-Like Receptor 9</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Expression des gènes</term><term>Rats</term><term>Récepteur-9 de type Toll-like</term><term>Souris</term><term>Synergie des médicaments</term><term>Techniques de transfert de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although the CpG DNA immune response mediated by Toll-like receptor 9 (TLR9) has been extensively studied in a number of immune cells, the response to CpG DNA in endothelial cells (EC) is not well understood. In this study, we show that both mouse and rat lung EC display constitutive expression of TLR9 mRNA. Exposure to CpG DNA induced a potent proinflammatory response as manifested by an increased expression of IL-8 and ICAM-1 in mouse pulmonary EC. The proinflammatory response was sensitive to chloroquine, consistent with a role of endosomal contribution. A role for p38 MAPK and NF-kappaB pathway was apparent as the response was sensitive to inhibitors of p38 MAPK and NF-kappaB but was not affected by inhibitors of ERK1/2. A synergistic effect of CpG DNA and LPS on the inflammatory response is consistent with multiple TLR interaction in EC. This study suggests a possible role for CpG DNA-mediated EC immune response in the host defense system. It also has important implications in plasmid DNA-mediated pulmonary endothelium gene transfer.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region></list><tree><noCountry><name sortKey="Li, Song" sort="Li, Song" uniqKey="Li S" first="Song" last="Li">Song Li</name><name sortKey="Ma, Zheng" sort="Ma, Zheng" uniqKey="Ma Z" first="Zheng" last="Ma">Zheng Ma</name><name sortKey="Pitt, Bruce" sort="Pitt, Bruce" uniqKey="Pitt B" first="Bruce" last="Pitt">Bruce Pitt</name><name sortKey="Stevens, Troy" sort="Stevens, Troy" uniqKey="Stevens T" first="Troy" last="Stevens">Troy Stevens</name><name sortKey="Tang, Zhi Lue" sort="Tang, Zhi Lue" uniqKey="Tang Z" first="Zhi-Lue" last="Tang">Zhi-Lue Tang</name></noCountry><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Li, Jiang" sort="Li, Jiang" uniqKey="Li J" first="Jiang" last="Li">Jiang Li</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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