B6 cg tg cag cre esr1 5amc j mice

Casp1^−/− were kindly provided by Dr. Thirumala-Devi Kanneganti (St. Jude Children's Research Hospital). Cre-ER^TM (B6.Cg-Tg(CAG-cre/Esr1*)5Amc/J) mice and lysozyme M-Cre mice were purchased from The Jackson Laboratory (Sacramento, CA). Nlrp3^fl(D301N)/+ mice were kindly provided by Dr. Hal Hoffman (University of California, San Diego), and have been previously described (52 (link), 54 (link), 85 (link)). Nlrp3^CA/+ mice with constitutive activation of NLRP3 in myeloid cells driven by lysozyme M-Cre have been previously described (54 (link)). Cre-ER^TM mice and Nlrp3^fl(D301N)/+ mice were crossed to generate Nlrp3^fl(D301N)/+;Cre-ER^TM mice and Cre-ER^TM mice. Injection of tamoxifen (i.p., 75 mg/kg body weight; Sigma-Aldrich) to Nlrp3^fl(D301N)/+;Cre-ER^TM mice and Cre-ER^TM mice to yield inducible Nlrp3^CA (iNlrp3^CA) mice and control mice, respectively, has been previously described (85 (link)). Gsdmd^−/− mice were kindly provided by Dr. V. M. Dixit (Genentech, South San Francisco, CA). Asc-citrine and Gsdme^−/− mice were purchased from The Jackson Laboratory (Sacramento, CA). All mice were on the C57BL6J background and mouse genotyping was performed by PCR. All procedures were approved by the Institutional Animal Care and Use Committee of Washington University School of Medicine in St. Louis.

B6.Cg-Tg(CAG-cre/Esr1)5Amc/J mice, which we referred to as CAG-Cre^ERT2 mice were obtained from Jackson Laboratories (21 (link)). The B6.129S4-^{Meox2tm1(cre)Sor}/J mice, which we referred to as Meox-Cre, were kindly provided by Michelle Tallquist (24 (link)). Tg2576 mice were obtained from Taconic (38 (link)). Animals were group-housed in a standard 12-h light cycle and fed ad libitum standard mouse chow. All animal care protocols were followed in accordance with the Institutional Animal Care and Use Committee of the University of Texas Southwestern Medical Center and the University of Freiburg.
In light of the complexity of the genetic crosses and the different origin of the animal strains involved in this study, it has not been possible to conduct all experiments on a strictly homogenous C57BL/6 strain background. To ensure a minimal effect of strain background on the behavioral results we have found, all animals that were compared were brother/sister crosses that only differ by the absence or presence of Cre recombinase. Moreover, discovering a robust response like the one discussed here in a mixed background, as opposed to an inbred one, further strengthens the validity of the conclusions, rather than diminishing them. Most importantly perhaps, it further supports the applicability of the results to the even more genetically heterogeneous human population.