Tissue-specific role for IKKβ in Streptococcal pneumonia. (A) IKKβ^ΔEpi and IKKβ^f/f-Otet-cre control mice were infected intranasally with 5 × 10⁶ CFUs GBS in PBS. Bronchialveolar lavage was performed after 4 h, and CFUs were determined by serial dilution on Todd-Hewitt agar plates (n = 11–14; *, P = 0.0242). (B) Hematoxylin and eosin stain (left, H+E) of lungs from GBS-infected mice after 4 h showed reduced leukocyte infiltration in IKKβ^ΔEpi mice (arrows). Gram stain (right) of infected lungs showed accumulation of bacteria in alveolar spaces of IKKβ^ΔEpi lungs (arrows). Representative panels are shown from n = 8. Bar, 100 μm. (C) IKKβ^ΔMye and IKKβ^f/f control mice were infected as described above, and BAL CFUs were measured at 4 h (n = 11–14; *, P = 0.0304). (D) Hematoxylin and eosin stain of lungs from GBS-infected mice after 4 and 24 h showed resolution of peribronchial inflammation in the lungs of IKKβ^f/f mice at 24 h (top, arrows); however, inflammation in IKKβ^ΔMye mice fails to resolve (bottom, arrows). Bar, 200 μm. (E) PMN recruitment in IKKβ^ΔMye and IKKβ^f/f mice infected with GBS was counted under high power field after hematoxylin and eosin stain. Data are represented as mean ± SEM of n = 8 (**, P = 0.005).