Figure 1

The magnitude of IAV lung inflammation is reduced in Ndst1f/f CD11cCre + mutant mice, with inhibition in inflammation compared to that in Ndst1f/f CD11cCre− wildtype controls at day 9 post-inoculation. Mutant and wildtype mice were inoculated with an intranasal dose of 20 PFU of PR8 IAV (n = 5 mutant and n = 6 wildtype). At day 9 post-inoculation (p.i.) lungs were harvested, inflated, paraffin embedded, and sectioned. (A) Representative images of H&E-stained lung sections from IAV-infected Ndst1f/f CD11cCre− wildtype mice are shown, with representative 400X photomicrographs from inflammatory zones shown below each section (scale bar = 1 mm for low-power whole-lung images; bar = 50 μm for 400X photomicrographs). (B) Images of H&E-stained lung sections and representative photomicrographs from IAV-infected Ndst1f/f CD11cCre + mutant mice. (C) Histopathology from lung sections was analyzed by a trained pathologist blinded to genotype; and mean inflammatory index for each lung (estimated on a 0–3 scale of severity by the pathologist) was normalized from inflammatory scores of inflamed areas on lung sections. Inflammatory indices were assessed through analyses of both pathologic intensity of inflammation (left) as well as the mean spatial inflammatory involvement of lung sections (right). Spatial inflammatory involvement for any given lung section (percentage of section with any inflammation) was also initially determined through quantification by counting blinded to genotype. Mean +/− SD for the measures normalized to wildtype is shown on the graph (*P = 0.03 and *P = 0.02 for differences in means for intensity and spatial measures, respectively).