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Figure 1 | Particle and Fibre Toxicology

Figure 1

From: Interleukin-12 is not essential for silicosis in mice

Figure 1

Pathology in wild-type and IL-12 knock-out Mice. This figure illustrates the lung pathology of C57Bl/6 wild-type and IL-12 KO mice 112 days after inhalation exposure to sham-air, rutile titanium dioxide, or cristobalite silica. A lung section from an air-exposed mouse shows normal histology (A, H&E, 400×). A lung section from a mouse exposed to TiO2 (B, H&E, 400×) shows increased numbers of macrophages, and many of these cells are laden with particulates. No inflammatory foci are present, and the alveolar walls appear normal. Tissue from wild-type mice exposed to silica (C, H&E, 200×; D, H&E, 400×) show numerous patchy collections of macrophages and lymphocytes, with apparent hyperplastic alveolar epithelial cells and fibroblasts. Cuffs of lymphocytes surround some arterioles and airways. Trichrome stain reveals bright blue connective tissue matrix and collagen (arrows) beneath the epithelium of the bronchial wall in a section from a sham-air exposed mouse (E), but rare matrix staining in the alveolar septae (400×). A silica-exposed lung (F) shows bright blue trichrome stained matrix in alveolar walls (arrows) within a silicotic lesion (400×). Sections from silica-exposed IL-12 KO mice show typical features of silicosis (G, H&E, 200×; H, H&E, 400×). The extent and features of disease are as intense as those found in the wild-type silica-exposed mice.

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