Our laboratory has previously described the Sp19 model, involving a focal pneumonia in which pulmonary antibacterial defenses are strongly dependent upon effective inflammatory responses, as evidenced by defective immunity and excessive bacterial outgrowth in mice with whole animal lack of RelA [59], lack of myeloid RelA [52], lack of alveolar epithelial RelA [67], disruption of TNF- α and IL-1 signaling [61], or ablation of the acute phase response [68]. This evidence concerns the gene IL1B and susceptibility to pneumonia measurement.