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We read with great interest the article by Stoecklein et al. (1), in which the authors showed that inflammasome activation was induced in immune cells, including macrophages, isolated from mice exposed to whole body irradiation. They further showed that both Nlrp3−/− and caspase-1−/− mice showed lower IL-1β production and inflammatory responses to radiation exposure than wild-type mice. Interestingly, however, immune cells from Nlrp3−/− mice showed substantial levels of caspase-1 activation that were not indistinguishable from wild-type mice. Although the results of this study are rather puzzling, they provide two important insights. First, radiation-induced IL-1β production is mediated through the NLRP3 protein independently of the inflammasomes. In this regard, we recently demonstrated that NLRP3 regulates neutrophil functions and contributes to the pathogenesis of hepatic ischemia-reperfusion injury (2) and hyperoxic acute lung injury independently of the inflammasomes (3). Therefore, it remains to be examined whether neutrophil-derived serine proteases, such as neutrophil elastase and proteinase 3, are involved in radiation-induced pro–IL-1β processing and its mature form production. Second, the study by Stoecklein et al. (1) also suggests that other inflammasomes, except for NLRP3 inflammasomes, might be involved in radiation-mediated caspase-1 activation. Because radiation can damage intestinal integrity and influence the intestinal flora (4), we assume that other inflammasome complexes (e.g., NLRP1, NLRC4, and AIM2 inflammasomes) that can recognize pathogen-associated molecular patterns are activated in radiation-mediated caspase-1 activation.

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