Figure 1. Targeted injury to type II AEC promotes lung inflammation.

Diphtheria toxin was administered daily for 14 days to either WT (DTR−) or DTR+ mice. (A) Lung cells from individual mice were isolated from untreated mice (D0) and at 7, 14, and 21 days after the onset of DT treatment. Cells were antibody-stained and flow cytometric analysis was used to identify and enumerate total numbers of CD45+ lung leukocytes. Data are mean ± SEM of 8–12 DT-treated mice per time point (from three separate experiments) assayed individually; DTR+ mice, black squares and solid lines; WT mice, gray triangles and dashed lines; * p<0.05 vs. Day 0 (uninfected) of mice of the same DTR expression profile; ** p<0.05 when values from WT mice or DTR+ mice were compared against each other at the designated time point. (B) Representative photomicrographs of lung sections (H & E staining; 40x objective) obtained from DT-treated WT (left panel) and DTR+ mice (right panel and inset). Note the presence of increased cellularity in the alveolar regions of DTR+ mice with evidence of large cells both with alveolar airspaces (inset; orange arrows) and within thickened interstitial infiltrates (inset; green arrows). (C) A limited gene array was performed on RNA extracted from enriched lung leukocyte populations of WT mice (circles) or DTR+ mice (squares) following 14 days of DT-treatment. Data is plotted as the cycle time difference (ΔCt) between the target gene and the β-actin gene. Solid arrows indicate significant differences in gene expression between WT and DTR+ mice.