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| Reference : Overexpression of CD39 in mouse airways promotes bacteria induced inflammation |
| Scientific journals : Article | |||
| Human health sciences : Immunology & infectious disease | |||
| http://hdl.handle.net/2268/126224 | |||
| Overexpression of CD39 in mouse airways promotes bacteria induced inflammation | |
| English | |
| [fr] Une augmentation de l'expression de CD39 dans les voies respiratoires murines favorise l'inflammation en réponse à une infection bactérienne | |
| Theatre, Emilie [Université de Liège - ULg > Département de productions animales > GIGA-R : Génomique animale >] | |
| Frederix, Kim [Université de Liège - ULg > Sciences Biomédicales et Précliniques > Génétique Humaine > >] | |
| Guilmain, William [Université de Liège - ULg > Sciences Biomédicales et Précliniques > Génétique Humaine > >] | |
| Delierneux, Céline [Université de Liège - ULg > Département des sciences biomédicales et précliniques > GIGA-R : Génétique humaine >] | |
| Lecut, Christelle [Université de Liège - ULg > Département des sciences biomédicales et précliniques > GIGA-R : Génétique humaine >] | |
| Bettendorff, Lucien [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biochimie et physiologie humaine et pathologique >] | |
| BOURS, Vincent [Centre Hospitalier Universitaire de Liège - CHU > > Génétique >] | |
Oury, Cécile  [Université de Liège - ULg > Département des sciences biomédicales et précliniques > GIGA-R : Génétique humaine >] | |
| Aug-2012 | |
| Journal of Immunology | |
| American Association of Immunologists | |
| 189 | |
| 4 | |
| 1966-1974 | |
| International | |
| 0022-1767 | |
| 1550-6606 | |
| Baltimore | |
| MD | |
| [en] transgenic mice ; airway inflammation ; bacteria infection | |
| [en] In airways, the ecto-nucleoside triphosphate diphosphohydrolase CD39 plays a central role in the regulation of physiological mucosal nucleotide concentrations and likely contributes to the control of inflammation because accelerated ATP metabolism occurs in chronic inflammatory lung diseases.We sought to determine whether constant elevated CD39 activity in lung epithelia is sufficient to cause inflammation and whether this affects the response to acute LPS or Pseudomonas aeruginosa exposure. We generated transgenic mice overexpressing human CD39 under the control of the airway-specific Clara cell 10-kDa protein gene promoter.
Transgenic mice did not develop any spontaneous lung inflammation. However, intratracheal instillation of LPS resulted in accelerated recruitment of neutrophils to the airways of transgenic mice. Macrophage clearance was delayed, and the amounts of CD8+ T and B cells were augmented. Increased levels of keratinocyte chemoattractant, IL-6, and RANTES were produced in transgenic lungs. Similarly, higher numbers of neutrophils and macrophages were found in the lungs of transgenic mice infected with P. aeruginosa, which correlated with improved bacteria clearance. The transgenic phenotype was partially and differentially restored by coinstillation of P2X1 or P2X7 receptor antagonists or of caffeine with LPS. Thus, a chronic increase of epithelial CD39 expression and activity promotes airway inflammation in response to bacterial challenge by enhancing P1 and P2 receptor activation. | |
| Giga-Cardiovascular Sciences | |
| http://hdl.handle.net/2268/126224 | |
| 10.4049/jimmunol.1102600 |
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