Fig. 1
From: NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis

Silica particles persist in the lung, causing chronic inflammation, nodule formation, and fibrosis. (A-D) Groups of 5 C57BL/6J mice were intranasally administered 2 mg of silica. Control mice received PBS alone. Data are representative of at least 2 independent experiments. (A) Schematic of disease progression following silica delivery. (B) Cytospin analysis of H&E-stained bronchoalveolar lavage (BAL) at day 3. Representative brightfield images (top panels). Arrows indicate the presence of immune cells with morphology resembling neutrophils (N), lymphocytes (L), and macrophages (M) cells. The boxed area demonstrates macrophages containing silica crystals, providing a magnified view. Silica particles in the same field of view were additionally visualized under polarized light (bottom panels). 400x magnification (scale bar 100 μm). (C) Visualization of silica at day 14 in formalin-fixed lung tissue sections using multiphoton microscopy. 25x magnification (scale bar 100 μm). Yellow arrows indicate silica. Extracellular matrix (ECM), airways, and arteries are indicated. (D) Representative images of Masson’s trichrome-stained, formalin-fixed lung tissue sections at day 14 and 28. 40x magnification (scale bar 100 μm). Gross histological changes characteristic of silicosis were observed. Silicotic nodules are indicated by the arrows