Fig. 1

CCR2^−/− mice show increased susceptibility to low dose aerosol HN878 infection. B6 and CCR2^−/− mice were aerosol-infected with ~100 CFU of a H37Rv, b CDC1551, c T17x, d HN878, or e HN563. Bacterial burden in the lung and spleen was determined by plating a–c, e at 30 dpi or d at different dpi. f Lung myeloid cell populations were enumerated in B6 and CCR2^−/− HN878-infected mice using flow cytometry at indicated dpi. g–k Pulmonary histology was assessed on FFPE lung sections from 30, 60, and 100 dpi samples stained with g Trichrome staining or j H&E staining. h Inflammatory area expressing collagen was quantified using Visiomorph image processing software to determine lung fibrosis. i RNA was extracted from B6 and CCR2^−/− HN878-infected lungs and relative mRNA expression of specific genes was determined by qRT-PCR. Gapdh was used as internal control. k Inflammation was quantified using the morphometric tool of the Zeiss Axioplan microscope to determine the total number of granulomas per lobe. l The total number of CD11c⁺ Mtb containing cells per 200× was determined by counting in FFPE lung sections of B6 and CCR2^−/− mice. AMs alveolar macrophages, RMs recruited macrophages, Monos monocytes, mDCs myeloid dendritic cells, Neuts neutrophils. n = 5, a–e Student’s t-test between B6 and CCR2^−/−, f 2-way ANOVA with Bonferroni’s post test. h–l Student’s t-test was used to determine differences per time point