NLRP3 promotes inflammation-induced skin cancer but is dispensable for asbestos-induced mesothelioma.

Détails

ID Serval
serval:BIB_03A1F1D8B870
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
NLRP3 promotes inflammation-induced skin cancer but is dispensable for asbestos-induced mesothelioma.
Périodique
Immunology and Cell Biology
Auteur(s)
Chow M.T., Tschopp J., Möller A., Smyth M.J.
ISSN
1440-1711 (Electronic)
ISSN-L
0818-9641
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
90
Numéro
10
Pages
983-986
Langue
anglais
Notes
Publication types: Journal Article
pdf: Short Communication
Résumé
Asbestos exposure can result in serious and frequently lethal diseases, including malignant mesothelioma. The host sensor for asbestos-induced inflammation is the NLRP3 inflammasome and it is widely assumed that this complex is essential for asbestos-induced cancers. Here, we report that acute interleukin-1β production and recruitment of immune cells into peritoneal cavity were significantly decreased in the NLRP3-deficient mice after the administration of asbestos. However, NLRP3-deficient mice displayed a similar incidence of malignant mesothelioma and survival times as wild-type mice. Thus, early inflammatory reactions triggered by asbestos are NLRP3-dependent, but NLRP3 is not critical in the chronic development of asbestos-induced mesothelioma. Notably, in a two-stage carcinogenesis-induced papilloma model, NLRP3-deficient mice showed a resistance phenotype in two different strain backgrounds, suggesting a tumour-promoting role of NLRP3 in certain chemically-induced cancer types.
Pubmed
Web of science
Création de la notice
31/12/2012 12:16
Dernière modification de la notice
20/08/2019 12:25
Données d'usage