Silicosis is an occupational lung BMS-907351 customer reviews disease resulting from chronic inhalation of dust containing silica dioxide. It is characterized by persistent inflammation, fibroblast proliferation and excessive collagen deposition, resulting in interstitial fibrosis. During the development of silicosis, contact between alveolar macrophages and silica drives the subsequent steps. The uptake of silica particles by macrophages triggers the production of reactive oxygen species via the oxidative stress pathway, which in turn contributes to pulmonary damage and macrophage death by apoptosis. Sustained ROS generation perpetuates the continuum of phagocytosis, cell death, inflammatory cell recruitment and silica deposition, and is responsible for progressive and irreversible lung injury. The fibrosis and the inflammatory reaction inside the alveolar spaces lead to respiratory failure due to a reduction in the area of gas exchange and impairment of lung function. As yet, no curative treatment exists for silicosis. Clinical management is directed at controlling symptoms and preventing complications. Therefore, transplantation of stem cells obtained from several sources has been proposed. In this context, an increasing number of articles have demonstrated the efficacy of either systemic or intratracheal administration of bone marrow cells in several lung injury animal models. This includes mouse models of acute lung injury and fibrosis, sepsis, ischemia/reperfusion injury, asthma, chronic obstructive pulmonary disease, and other pulmonary diseases. It has been shown that bone marrow-derived cells are capable of promoting re-epithelization of lung parenchyma, modulating immune responses, and decreasing fibrosis. However, few studies have been done in the setting of a chronic persistent inflammatory and fibrotic condition such as silicosis. Maron-Gutierrez et al. reported that bone marrow mononuclear cells had a preventive effect when infused 1 h after the introduction of silica, with improvement in lung function, inflammation, and fibrosis 15 days after the start of the protocol. However, these effects were only partially reversed in a longer follow-up in a protocol with infusion of bone marrow-derived cells by the intratracheal route in animals with a 15-day silica-induced injury. Therefore, we asked if treatment with BMMCs in the chronic stages of murine silicosis could also have beneficial effects on lung function and structure. Silicosis is a chronic fibrotic disorder that progressively leads to respiratory failure. Chronic inhalation of silica particles leads to cycles of cell activation, silica particle phagocytosis, cell death, and release of inflammatory/profibrotic mediators such as cytokines, arachidonic acid metabolites.