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Abstract
Alveolar macrophages (AMs) play an important defensive role by removing dust and bacteria from alveoli. Apoptosis of AMs is associated with lung fibrosis; however, the relationship between this apoptotic event and environmental factors, such as the presence of lipopolysaccharides (LPSs) in the workplace, has not yet been addressed. To investigate whether exposure to LPS can exacerbate fibrosis, we collected AMs from 12 male workers exposed to silica and incubated them in the presence and absence of LPS for 24 h. We show that the levels of cleaved caspase-3 and pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha were increased in these AMs following LPS treatment. Moreover, we demonstrate that LPS exposure aggravated apoptosis and the release of inflammatory factors in AMs in a mouse model of silicosis, which eventually promoted pulmonary fibrosis. These results suggest that exposure to LPS may accelerate the progression of pulmonary fibrosis in silicosis by increasing apoptosis and inflammation in AMs.
Highlights
Silicosis, characterized by extensive pulmonary nodular fibrosis, is the most common type of pneumoconiosis [1] and is caused by the prolonged exposure to a high quality of free silica dust [2]
We found that LPS treatment increased apoptosis and the release of inflammatory factors in Alveolar macrophages (AMs) from silica-exposed workers, in addition to aggravating pulmonary fibrosis in a mouse model of silicosis
Twelve male silica-exposed workers were selected for the present study and divided into two groups: six observers, whose X-ray images showed uncertain silicosis-like changes, the nature and severity of which did not dramatically change within 5 years; and six silicosis patients, whose disease was identified by X-ray images
Summary
Silicosis, characterized by extensive pulmonary nodular fibrosis, is the most common type of pneumoconiosis [1] and is caused by the prolonged exposure to a high quality of free silica dust [2]. Alveolar macrophages (AMs) play an important defensive role in the progression of silicosis [5]. The released SiO2 is captured by other AMs, and this process is repeated, leading to the aggravation of silicosis [6–8]. There is increasing evidence that LPS can aggravate a variety of diseases, such as Alzheimer’s disease and Parkinson’s disease, reproductive system damage, and liver toxicity, by promoting apoptosis and inflammation [10–13]. A previous study detected LPS in the bronchoalveolar lavage fluid of silicosis patients [9]. There is an urgent need to elucidate whether LPS can stimulate the progression of pulmonary fibrosis in silicosis
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