We study the mechanisms that drive silicosis using both in-vitro and in-vivo models. In our laboratory, we use in-vitro systems such as lung epithelial cells, fibroblasts, and immune cells to understand how silica particles trigger inflammation and fibrotic signalling. These models let us pinpoint molecular pathways and test potential treatments in a controlled setting. To complement this work, we use in-vivo models, where exposure to silica dust reproduces many of the key features of human disease, including persistent lung inflammation, granuloma formation, and scarring. By combining these approaches, we can explore how silicosis develops at both the cellular and whole-organ level, giving us a clearer picture of the disease and how it might be prevented or treated.