Fig. 6

Depletion of CCR2⁺ cells at the time of AM egress from airways increases susceptibility to HN878 infection. CCR2-DTR mice (n = 4) were infected with HN878 and administered Dtx a–c IP at 12, 14, and 16 dpi or d–f at −1, 1, and 3 dpi. a, d Lung bacterial burden was determined by plating on 30 dpi. b, e Neutrophil, AM, monocyte, and RM numbers were determined in PBS-treated and Dtx-treated CCR2-DTR mice at 30 dpi. c, f Pulmonary histology was assessed on FFPE lung sections stained with H&E, and inflammatory area was quantified using the morphometric tool of the Zeiss Axioplan microscope. g B6 (n = 5) and CCR2^−/− mice (n = 8 per group) were infected with HN878, and CCR2^−/− mice received either PBS or HN878-stimulated BMDMs delivered IT on 15 and 21 dpi. Lungs were harvested at 30 dpi and bacterial burden was determined by plating. Neuts neutrophils, AMs alveolar macrophages, Monos monocytes, RMs recruited macrophages. a–f Student’s t-test. g 1-Way ANOVA with Tukey’s post test