Bacterial DNA induces pulmonary damage via TLR-9 through cross-talk with neutrophils.
Identifieur interne : 001477 ( Main/Exploration ); précédent : 001476; suivant : 001478Bacterial DNA induces pulmonary damage via TLR-9 through cross-talk with neutrophils.
Auteurs : Kiyoshi Itagaki [États-Unis] ; Yasaman Adibnia ; Shiqin Sun ; Cong Zhao ; Tolga Sursal ; Yu Chen ; Wolfgang Junger ; Carl J. HauserSource :
- Shock (Augusta, Ga.) [ 1540-0514 ] ; 2011.
Descripteurs français
- KwdFr :
- ADN bactérien (pharmacologie), Adhérence cellulaire (), Adhérence cellulaire (physiologie), Cellules cultivées, Cellules endothéliales (), Cellules endothéliales (cytologie), Endothélium vasculaire (), Endothélium vasculaire (cytologie), Endothélium vasculaire (métabolisme), Granulocytes neutrophiles (cytologie), Granulocytes neutrophiles (métabolisme), Humains, Lignée cellulaire, Molécule-1 d'adhérence intercellulaire (génétique), Molécule-1 d'adhérence intercellulaire (métabolisme), Récepteur-9 de type Toll-like (génétique), Récepteur-9 de type Toll-like (métabolisme), Sélectine E (génétique), Sélectine E (métabolisme).
- MESH :
- cytologie : Cellules endothéliales, Endothélium vasculaire, Granulocytes neutrophiles.
- génétique : Molécule-1 d'adhérence intercellulaire, Récepteur-9 de type Toll-like, Sélectine E.
- métabolisme : Endothélium vasculaire, Granulocytes neutrophiles, Molécule-1 d'adhérence intercellulaire, Récepteur-9 de type Toll-like, Sélectine E.
- pharmacologie : ADN bactérien.
- physiologie : Adhérence cellulaire.
- Adhérence cellulaire, Cellules cultivées, Cellules endothéliales, Endothélium vasculaire, Humains, Lignée cellulaire.
English descriptors
- KwdEn :
- CD11b Antigen (genetics), CD11b Antigen (metabolism), CD18 Antigens (genetics), CD18 Antigens (metabolism), Cell Adhesion (drug effects), Cell Adhesion (physiology), Cell Line, Cells, Cultured, DNA, Bacterial (pharmacology), E-Selectin (genetics), E-Selectin (metabolism), Endothelial Cells (cytology), Endothelial Cells (drug effects), Endothelium, Vascular (cytology), Endothelium, Vascular (drug effects), Endothelium, Vascular (metabolism), Humans, Intercellular Adhesion Molecule-1 (genetics), Intercellular Adhesion Molecule-1 (metabolism), Neutrophils (cytology), Neutrophils (metabolism), Toll-Like Receptor 9 (genetics), Toll-Like Receptor 9 (metabolism).
- MESH :
- chemical , genetics : CD11b Antigen, CD18 Antigens, E-Selectin, Intercellular Adhesion Molecule-1, Toll-Like Receptor 9.
- chemical , metabolism : CD11b Antigen, CD18 Antigens, E-Selectin, Intercellular Adhesion Molecule-1, Toll-Like Receptor 9.
- cytology : Endothelial Cells, Endothelium, Vascular, Neutrophils.
- drug effects : Cell Adhesion, Endothelial Cells, Endothelium, Vascular.
- metabolism : Endothelium, Vascular, Neutrophils.
- chemical , pharmacology : DNA, Bacterial.
- physiology : Cell Adhesion.
- Cell Line, Cells, Cultured, Humans.
Abstract
Bacterial DNA (bDNA) contains hypomethylated "CpG" repeats that can be recognized by Toll-like receptor 9 (TLR-9) as a pathogen-associated molecular pattern. The ability of bDNA to initiate lung injury via TLR-9 has been inferred on the basis of studies using artificial CpG DNA. But the role of authentic bDNA in lung injury is still unknown. Moreover, the mechanisms by which CpG DNA species can lead to pulmonary injury are unknown, although neutrophils (PMNs) are thought to play a key role in the genesis of septic acute lung injury. We evaluated the effects of bDNA on PMN-endothelial cell (EC) interactions thought critical for initiation of acute lung injury. Using a biocapacitance system to monitor real-time changes in endothelial permeability, we demonstrate here that bDNA causes EC permeability in a dose-dependent manner uniquely in the presence of PMNs. These permeability changes are inhibited by chloroquine, suggesting TLR-9 dependency. When PMNs were preincubated with bDNA and applied to ECs or when bDNA was applied to ECs without PMNs, no permeability changes were detected. To study the underlying mechanisms, we evaluated the effects of bDNA on PMN-EC adherence. Bacterial DNA significantly increased PMN adherence to ECs in association with upregulated adhesion molecules in both cell types. Taken together, our results strongly support the conclusion that bDNA can initiate lung injury by stimulating PMN-EC adhesive interactions predisposing to endothelial permeability. Bacterial DNA stimulation of TLR-9 appears to promote enhanced gene expression of adhesion molecules in both cell types. This leads to PMN-EC cross-talk, which is required for injury to occur.
DOI: 10.1097/SHK.0b013e3182369fb2
PubMed: 21937948
Affiliations:
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Le document en format XML
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Hauser</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21937948</idno><idno type="pmid">21937948</idno><idno type="doi">10.1097/SHK.0b013e3182369fb2</idno><idno type="wicri:Area/PubMed/Corpus">000374</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000374</idno><idno type="wicri:Area/PubMed/Curation">000374</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000374</idno><idno type="wicri:Area/PubMed/Checkpoint">000374</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000374</idno><idno type="wicri:Area/Ncbi/Merge">000160</idno><idno type="wicri:Area/Ncbi/Curation">000160</idno><idno type="wicri:Area/Ncbi/Checkpoint">000160</idno><idno type="wicri:Area/Main/Merge">001479</idno><idno type="wicri:Area/Main/Curation">001477</idno><idno type="wicri:Area/Main/Exploration">001477</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Bacterial DNA induces pulmonary damage via TLR-9 through cross-talk with neutrophils.</title><author><name sortKey="Itagaki, Kiyoshi" sort="Itagaki, Kiyoshi" uniqKey="Itagaki K" first="Kiyoshi" last="Itagaki">Kiyoshi Itagaki</name><affiliation wicri:level="1"><nlm:affiliation>Department of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. kitagaki@bidmc.harvard.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215</wicri:regionArea><wicri:noRegion>Massachusetts 02215</wicri:noRegion></affiliation></author><author><name sortKey="Adibnia, Yasaman" sort="Adibnia, Yasaman" uniqKey="Adibnia Y" first="Yasaman" last="Adibnia">Yasaman Adibnia</name></author><author><name sortKey="Sun, Shiqin" sort="Sun, Shiqin" uniqKey="Sun S" first="Shiqin" last="Sun">Shiqin Sun</name></author><author><name sortKey="Zhao, Cong" sort="Zhao, Cong" uniqKey="Zhao C" first="Cong" last="Zhao">Cong Zhao</name></author><author><name sortKey="Sursal, Tolga" sort="Sursal, Tolga" uniqKey="Sursal T" first="Tolga" last="Sursal">Tolga Sursal</name></author><author><name sortKey="Chen, Yu" sort="Chen, Yu" uniqKey="Chen Y" first="Yu" last="Chen">Yu Chen</name></author><author><name sortKey="Junger, Wolfgang" sort="Junger, Wolfgang" uniqKey="Junger W" first="Wolfgang" last="Junger">Wolfgang Junger</name></author><author><name sortKey="Hauser, Carl J" sort="Hauser, Carl J" uniqKey="Hauser C" first="Carl J" last="Hauser">Carl J. Hauser</name></author></analytic><series><title level="j">Shock (Augusta, Ga.)</title><idno type="eISSN">1540-0514</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>CD11b Antigen (genetics)</term><term>CD11b Antigen (metabolism)</term><term>CD18 Antigens (genetics)</term><term>CD18 Antigens (metabolism)</term><term>Cell Adhesion (drug effects)</term><term>Cell Adhesion (physiology)</term><term>Cell Line</term><term>Cells, Cultured</term><term>DNA, Bacterial (pharmacology)</term><term>E-Selectin (genetics)</term><term>E-Selectin (metabolism)</term><term>Endothelial Cells (cytology)</term><term>Endothelial Cells (drug effects)</term><term>Endothelium, Vascular (cytology)</term><term>Endothelium, Vascular (drug effects)</term><term>Endothelium, Vascular (metabolism)</term><term>Humans</term><term>Intercellular Adhesion Molecule-1 (genetics)</term><term>Intercellular Adhesion Molecule-1 (metabolism)</term><term>Neutrophils (cytology)</term><term>Neutrophils (metabolism)</term><term>Toll-Like Receptor 9 (genetics)</term><term>Toll-Like Receptor 9 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN bactérien (pharmacologie)</term><term>Adhérence cellulaire ()</term><term>Adhérence cellulaire (physiologie)</term><term>Cellules cultivées</term><term>Cellules endothéliales ()</term><term>Cellules endothéliales (cytologie)</term><term>Endothélium vasculaire ()</term><term>Endothélium vasculaire (cytologie)</term><term>Endothélium vasculaire (métabolisme)</term><term>Granulocytes neutrophiles (cytologie)</term><term>Granulocytes neutrophiles (métabolisme)</term><term>Humains</term><term>Lignée cellulaire</term><term>Molécule-1 d'adhérence intercellulaire (génétique)</term><term>Molécule-1 d'adhérence intercellulaire (métabolisme)</term><term>Récepteur-9 de type Toll-like (génétique)</term><term>Récepteur-9 de type Toll-like (métabolisme)</term><term>Sélectine E (génétique)</term><term>Sélectine E (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>CD11b Antigen</term><term>CD18 Antigens</term><term>E-Selectin</term><term>Intercellular Adhesion Molecule-1</term><term>Toll-Like Receptor 9</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>CD11b Antigen</term><term>CD18 Antigens</term><term>E-Selectin</term><term>Intercellular Adhesion Molecule-1</term><term>Toll-Like Receptor 9</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales</term><term>Endothélium vasculaire</term><term>Granulocytes neutrophiles</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term><term>Endothelium, Vascular</term><term>Neutrophils</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Adhesion</term><term>Endothelial Cells</term><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Molécule-1 d'adhérence intercellulaire</term><term>Récepteur-9 de type Toll-like</term><term>Sélectine E</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelium, Vascular</term><term>Neutrophils</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Endothélium vasculaire</term><term>Granulocytes neutrophiles</term><term>Molécule-1 d'adhérence intercellulaire</term><term>Récepteur-9 de type Toll-like</term><term>Sélectine E</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>ADN bactérien</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>DNA, Bacterial</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Adhérence cellulaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Adhesion</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Cells, Cultured</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adhérence cellulaire</term><term>Cellules cultivées</term><term>Cellules endothéliales</term><term>Endothélium vasculaire</term><term>Humains</term><term>Lignée cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bacterial DNA (bDNA) contains hypomethylated "CpG" repeats that can be recognized by Toll-like receptor 9 (TLR-9) as a pathogen-associated molecular pattern. The ability of bDNA to initiate lung injury via TLR-9 has been inferred on the basis of studies using artificial CpG DNA. But the role of authentic bDNA in lung injury is still unknown. Moreover, the mechanisms by which CpG DNA species can lead to pulmonary injury are unknown, although neutrophils (PMNs) are thought to play a key role in the genesis of septic acute lung injury. We evaluated the effects of bDNA on PMN-endothelial cell (EC) interactions thought critical for initiation of acute lung injury. Using a biocapacitance system to monitor real-time changes in endothelial permeability, we demonstrate here that bDNA causes EC permeability in a dose-dependent manner uniquely in the presence of PMNs. These permeability changes are inhibited by chloroquine, suggesting TLR-9 dependency. When PMNs were preincubated with bDNA and applied to ECs or when bDNA was applied to ECs without PMNs, no permeability changes were detected. To study the underlying mechanisms, we evaluated the effects of bDNA on PMN-EC adherence. Bacterial DNA significantly increased PMN adherence to ECs in association with upregulated adhesion molecules in both cell types. Taken together, our results strongly support the conclusion that bDNA can initiate lung injury by stimulating PMN-EC adhesive interactions predisposing to endothelial permeability. Bacterial DNA stimulation of TLR-9 appears to promote enhanced gene expression of adhesion molecules in both cell types. This leads to PMN-EC cross-talk, which is required for injury to occur.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Adibnia, Yasaman" sort="Adibnia, Yasaman" uniqKey="Adibnia Y" first="Yasaman" last="Adibnia">Yasaman Adibnia</name><name sortKey="Chen, Yu" sort="Chen, Yu" uniqKey="Chen Y" first="Yu" last="Chen">Yu Chen</name><name sortKey="Hauser, Carl J" sort="Hauser, Carl J" uniqKey="Hauser C" first="Carl J" last="Hauser">Carl J. Hauser</name><name sortKey="Junger, Wolfgang" sort="Junger, Wolfgang" uniqKey="Junger W" first="Wolfgang" last="Junger">Wolfgang Junger</name><name sortKey="Sun, Shiqin" sort="Sun, Shiqin" uniqKey="Sun S" first="Shiqin" last="Sun">Shiqin Sun</name><name sortKey="Sursal, Tolga" sort="Sursal, Tolga" uniqKey="Sursal T" first="Tolga" last="Sursal">Tolga Sursal</name><name sortKey="Zhao, Cong" sort="Zhao, Cong" uniqKey="Zhao C" first="Cong" last="Zhao">Cong Zhao</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Itagaki, Kiyoshi" sort="Itagaki, Kiyoshi" uniqKey="Itagaki K" first="Kiyoshi" last="Itagaki">Kiyoshi Itagaki</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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