IL1B and pulmonary fibrosis: Briefly, silica particles induce macrophage activation and lesion, triggering the release of metalloproteinases, free radicals, pro-inflammatory mediators such as IL-1β, TNF-α, and TGF-βthrough activation of nuclear factor (NF)-κB pathway [25,26], which is responsible for the recruitment of more inflammatory cells to the site of injury and are involved in lung fibrosis [2].