Fig 2.

DEP exposure drives early inflammation in the lungs that is exacerbated in the context of infection. A-F, TNF-α, IFN-γ, keratinocyte chemoattractant/human growth-regulated oncogene (KC/GRO), macrophage inflammatory protein 2 (MIP-2), IL-1β, and IL-6 levels in lung homogenate were measured for mice subjected to pneumococcal infection only (P, black circles), pneumococcus-infected mice subjected to daily DEP exposure (P+DEPs, gray squares), and mice subjected to daily DEP exposure in the absence of infection (DEPs, white triangles). G, Representative images of lungs from sham-exposed (left) and DEP-exposed (right) mice at day 7 postinfection following hematoxylin and eosin staining. H-J, The number of neutrophils (CD45⁺Gr1⁺), macrophages (CD45⁺F4/80⁺CD11b⁺), and regulatory T cells (Tregs) (CD45⁺CD4⁺Foxp3⁺) in lung cell suspension was measured by flow cytometry for mice subjected to pneumococcal infection only (P, black circles), pneumococcus-infected mice subjected to daily DEP exposure (P+DEPs, gray squares) and mice subjected to daily DEP exposure in the absence of infection (DEPs, white triangles). The gating strategy is shown in Fig E2. Error bars indicate the SEM; ****P < .0001; ***P < .001; **P < .01; * P < .05. Scale bars represent 200 microns, n = 7 to 10 per group, per time point.