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NLRP3 promotes inflammation‐induced skin cancer but is dispensable for asbestos‐induced mesothelioma
Author(s) -
Chow Melvyn T,
Tschopp Jürg,
Möller Andreas,
Smyth Mark J
Publication year - 2012
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2012.46
Subject(s) - asbestos , mesothelioma , inflammation , medicine , cancer research , pathology , materials science , metallurgy
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.