In addition, Nlrp3-/—mice infected with ΔfliCΔsiiD exhibited increased bacterial burden in tissues and decreased fecal lipocalin-2, serum IL-1β and IL-18, in comparison with WT- or Nlrc4-/—mice infected with ΔfliCΔsiiD (Fig 11E–11K), indicating that NLRP3 plays a functionally essential role in response to ΔfliCΔsiiD infection. This evidence concerns the gene IL1B and infection.