Journal
IMMUNOLOGY AND CELL BIOLOGY
Volume 90, Issue 10, Pages 983-986Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/icb.2012.46
Keywords
asbestos; mesothelioma; inflammasome; inflammation; skin; cytokine
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Funding
- National Health and Medical Research Council (NH & MRC) of Australia Centre for Research Excellence in Asbestos Related Diseases
- NBCF Research Fellowship
- AICR
- Cancer Research Institute PhD Scholarship
- Swiss National Research Foundation, Institute for Arthritis Research, Apo-Sys consortium
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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-1 beta 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. Immunology and Cell Biology (2012) 90, 983-986; doi: 10.1038/icb.2012.46; published online 25 September 2012
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