Effects of poly(ADP-ribose) polymerase inhibition on inflammatory cell migration in a murine model of asthma.

Détails

ID Serval
serval:BIB_29EA62BB1252
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Effects of poly(ADP-ribose) polymerase inhibition on inflammatory cell migration in a murine model of asthma.
Périodique
Medical Science Monitor
Auteur⸱e⸱s
Virág L., Bai P., Bak I., Pacher P., Mabley J.G., Liaudet L., Bakondi E., Gergely P., Kollai M., Szabó C.
ISSN
1643-3750; 1234-1010
Statut éditorial
Publié
Date de publication
03/2004
Peer-reviewed
Oui
Volume
10
Numéro
3
Pages
BR77-BR83
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. Publication Status: ppublish
Résumé
BACKGROUND: Poly(ADP-ribose) polymerase-1 (PARP-1), a monomeric nuclear enzyme present in eukaryotes, plays a role in cell death, inflammatory mediator expression, and mononuclear cell recruitment in various experimental models of inflammation and reperfusion injury. Part of the molecular mechanism of this function involves the regulation of cytokine and chemokine production. Since chemokines are principal regulators of mononuclear and polymorphonuclear cell trafficking in asthma, we investigated the possibility whether PARP modulates chemokine production and cell recruitment in a murine model of asthma. MATERIAL/METHODS: We studied ovalbumin-sensitized mice challenged with a single dose of ovalbumin. RESULTS: PARP inhibition with the phenanthridinone-based PARP inhibitor PJ34 suppressed inflammatory cell migration. These effects were associated with downregulation of the CC chemokine MIP-1alpha, but not the CXC chemokine MIP-2. The production of TNF- alpha and IL-12, but not IL-5 or IL-13, was also suppressed by PARP inhibition. CONCLUSIONS: Our results demonstrate the pathogenetic role of PARP activation in a murine model of asthma. PARP selectively regulates the production of certain chemokines and cytokines in this experimental model, which may be responsible for some of the observed protective effects seen in the current murine asthma model.
Mots-clé
Animals, Asthma/drug therapy, Bronchoalveolar Lavage, Catalysis, Cell Death, Cell Movement, Chemokine CXCL2, Chemokines/metabolism, Cytokines/metabolism, Disease Models, Animal, Down-Regulation, Enzyme Inhibitors/pharmacology, Interleukin-10/metabolism, Interleukin-12/metabolism, Interleukin-13/metabolism, Interleukin-5/metabolism, Leukocytes, Mononuclear/metabolism, Lung/pathology, Male, Mice, Mice, Inbred BALB C, Ovalbumin/metabolism, Ovalbumin/pharmacology, Peroxidase/metabolism, Poly(ADP-ribose) Polymerases/antagonists & inhibitors, Time Factors, Tumor Necrosis Factor-alpha/metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 18:01
Dernière modification de la notice
20/08/2019 14:09
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