NLRP3 and infection: Secretion of these pro-inflammatory cytokines was completely abrogated in cells that were deficient in caspase-1/caspase-11, asc and nlrp3. Moreover, in an infection model, nlrp3-/- mice were less capable of controlling bacterial burden in some tissues (spleen) when compared to wild-type mice, indicating that the NLRP3 inflammasome has a role in recognizing R. australis infection and reducing pathogen burden [119].