To trial an inflammasome trigger that is less dependent upon NLRP3, we tested the response to the microbe C. difficile. C. difficile infection induces severe colitis due, in part, to the effects of the microbial glucosyltransferase toxin B (TcdB) on ASC function26,27. Measures of the production of IL-1β by BMDMs or macrophages isolated from the peritoneal cavity in response to either cultured C. difficile or the purified C. difficile TcdB toxin showed that ablating Zbtb16 impaired inflammasome activity (Fig. 2e). The loss of Zbtb16 also resulted in decreased cytotoxicity, as indicated by the release of LDH in response to C. difficile, its TcdB toxin or nigericin (Fig. 2f).
