Nonclassical pathway of Pseudomonas aeruginosa DNA-induced interleukin-8 secretion in cystic fibrosis airway epithelial cells.
Identifieur interne : 000417 ( PubMed/Checkpoint ); précédent : 000416; suivant : 000418Nonclassical pathway of Pseudomonas aeruginosa DNA-induced interleukin-8 secretion in cystic fibrosis airway epithelial cells.
Auteurs : M Nica A. Delgado [États-Unis] ; Jens F. Poschet ; Vojo DereticSource :
- Infection and immunity [ 0019-9567 ] ; 2006.
Descripteurs français
- KwdFr :
- ADN bactérien (pharmacologie), Biosynthèse des protéines, Cellules cultivées, Cellules épithéliales (immunologie), Chimiokines (biosynthèse), Concentration en ions d'hydrogène, Facteur de transcription NF-kappa B (physiologie), Humains, Interleukine-8 (biosynthèse), Mucoviscidose (immunologie), Mucoviscidose (microbiologie), Oligodésoxyribonucléotides (pharmacologie), Pseudomonas aeruginosa (génétique), Système de signalisation des MAP kinases, Transduction du signal (physiologie).
- MESH :
- biosynthèse : Chimiokines, Interleukine-8.
- génétique : Pseudomonas aeruginosa.
- immunologie : Cellules épithéliales, Mucoviscidose.
- microbiologie : Mucoviscidose.
- pharmacologie : ADN bactérien, Oligodésoxyribonucléotides.
- physiologie : Facteur de transcription NF-kappa B, Transduction du signal.
- Biosynthèse des protéines, Cellules cultivées, Concentration en ions d'hydrogène, Humains, Système de signalisation des MAP kinases.
English descriptors
- KwdEn :
- Cells, Cultured, Chemokines (biosynthesis), Cystic Fibrosis (immunology), Cystic Fibrosis (microbiology), DNA, Bacterial (pharmacology), Epithelial Cells (immunology), Humans, Hydrogen-Ion Concentration, Interleukin-8 (biosynthesis), MAP Kinase Signaling System, NF-kappa B (physiology), Oligodeoxyribonucleotides (pharmacology), Protein Biosynthesis, Pseudomonas aeruginosa (genetics), Signal Transduction (physiology).
- MESH :
- chemical , biosynthesis : Chemokines, Interleukin-8.
- genetics : Pseudomonas aeruginosa.
- immunology : Cystic Fibrosis, Epithelial Cells.
- microbiology : Cystic Fibrosis.
- chemical , pharmacology : DNA, Bacterial, Oligodeoxyribonucleotides.
- chemical , physiology : NF-kappa B, Signal Transduction.
- Cells, Cultured, Humans, Hydrogen-Ion Concentration, MAP Kinase Signaling System, Protein Biosynthesis.
Abstract
Pseudomonas aeruginosa is a critical colonizer of the respiratory tract in cystic fibrosis. The chronic infections with this microorganism contribute to excessive inflammation and progressive lung damage in cystic fibrosis patients. The full repertoire of Pseudomonas products that promote inflammation in the cystic fibrosis lung is not known. Here we show that P. aeruginosa DNA released from the bacterium, but not human DNA from epithelial cells or Escherichia coli DNA, displays proinflammatory properties and induces human respiratory epithelial cells to secrete interleukin-8 (IL-8), a key chemokine causing excessive neutrophil infiltration in the cystic fibrosis lung. IL-8 secretion was not due to an increase in NF-kappaB- or activator protein-1-dependent IL-8 promoter transcription, but instead depended on p38 and Erk mitogen-activated protein kinases. No secretion of IL-8 was observed using conventional Toll-like receptor 9 ligands (CpG oligonucleotides), although it could be demonstrated that parts of the Toll-like receptor 9-signaling pathway were functional, since class B and C CpG oligonucleotide ligands stimulated production of RANTES chemokine. The IL-8 secretion in response to P. aeruginosa DNA was decreased by treatments that inhibit acidification of intracellular organelles, using chloroquine, a pH-neutralizing compound, or bafilomycin A1, an inhibitor of vacuolar H+-ATPase. These data indicate that DNA released from P. aeruginosa during chronic infections may significantly contribute to the proinflammatory processes in cystic fibrosis. Our findings also show that treatments with drugs diminishing organellar acidification may reduce the inflammatory response in cystic fibrosis.
DOI: 10.1128/IAI.74.5.2975-2984.2006
PubMed: 16622236
Affiliations:
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The chronic infections with this microorganism contribute to excessive inflammation and progressive lung damage in cystic fibrosis patients. The full repertoire of Pseudomonas products that promote inflammation in the cystic fibrosis lung is not known. Here we show that P. aeruginosa DNA released from the bacterium, but not human DNA from epithelial cells or Escherichia coli DNA, displays proinflammatory properties and induces human respiratory epithelial cells to secrete interleukin-8 (IL-8), a key chemokine causing excessive neutrophil infiltration in the cystic fibrosis lung. IL-8 secretion was not due to an increase in NF-kappaB- or activator protein-1-dependent IL-8 promoter transcription, but instead depended on p38 and Erk mitogen-activated protein kinases. No secretion of IL-8 was observed using conventional Toll-like receptor 9 ligands (CpG oligonucleotides), although it could be demonstrated that parts of the Toll-like receptor 9-signaling pathway were functional, since class B and C CpG oligonucleotide ligands stimulated production of RANTES chemokine. The IL-8 secretion in response to P. aeruginosa DNA was decreased by treatments that inhibit acidification of intracellular organelles, using chloroquine, a pH-neutralizing compound, or bafilomycin A1, an inhibitor of vacuolar H+-ATPase. These data indicate that DNA released from P. aeruginosa during chronic infections may significantly contribute to the proinflammatory processes in cystic fibrosis. Our findings also show that treatments with drugs diminishing organellar acidification may reduce the inflammatory response in cystic fibrosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16622236</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0019-9567</ISSN><JournalIssue CitedMedium="Print"><Volume>74</Volume><Issue>5</Issue><PubDate><Year>2006</Year><Month>May</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Nonclassical pathway of Pseudomonas aeruginosa DNA-induced interleukin-8 secretion in cystic fibrosis airway epithelial cells.</ArticleTitle><Pagination><MedlinePgn>2975-84</MedlinePgn></Pagination><Abstract><AbstractText>Pseudomonas aeruginosa is a critical colonizer of the respiratory tract in cystic fibrosis. The chronic infections with this microorganism contribute to excessive inflammation and progressive lung damage in cystic fibrosis patients. The full repertoire of Pseudomonas products that promote inflammation in the cystic fibrosis lung is not known. Here we show that P. aeruginosa DNA released from the bacterium, but not human DNA from epithelial cells or Escherichia coli DNA, displays proinflammatory properties and induces human respiratory epithelial cells to secrete interleukin-8 (IL-8), a key chemokine causing excessive neutrophil infiltration in the cystic fibrosis lung. IL-8 secretion was not due to an increase in NF-kappaB- or activator protein-1-dependent IL-8 promoter transcription, but instead depended on p38 and Erk mitogen-activated protein kinases. No secretion of IL-8 was observed using conventional Toll-like receptor 9 ligands (CpG oligonucleotides), although it could be demonstrated that parts of the Toll-like receptor 9-signaling pathway were functional, since class B and C CpG oligonucleotide ligands stimulated production of RANTES chemokine. The IL-8 secretion in response to P. aeruginosa DNA was decreased by treatments that inhibit acidification of intracellular organelles, using chloroquine, a pH-neutralizing compound, or bafilomycin A1, an inhibitor of vacuolar H+-ATPase. These data indicate that DNA released from P. aeruginosa during chronic infections may significantly contribute to the proinflammatory processes in cystic fibrosis. Our findings also show that treatments with drugs diminishing organellar acidification may reduce the inflammatory response in cystic fibrosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Delgado</LastName><ForeName>Mónica A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, 915 Camino de Salud NE, Albuquerque, NM 87131, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Poschet</LastName><ForeName>Jens F</ForeName><Initials>JF</Initials></Author><Author ValidYN="Y"><LastName>Deretic</LastName><ForeName>Vojo</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI050825</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI050825</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI31193</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C408982">CPG-oligonucleotide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018925">Chemokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004269">DNA, 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