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.

中文翻译：

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脂多糖通过加重肺泡巨噬细胞凋亡和炎症促进矽肺肺纤维化

摘要 肺泡巨噬细胞 (AMs) 通过清除肺泡中的灰尘和细菌而发挥重要的防御作用。AMs 的凋亡与肺纤维化有关；然而，这种凋亡事件与环境因素（例如工作场所中脂多糖 (LPS) 的存在）之间的关系尚未得到解决。为了研究暴露于 LPS 是否会加剧纤维化，我们收集了 12 名暴露于二氧化硅的男性工人的 AM，并在存在和不存在 LPS 的情况下将他们培养 24 小时。我们表明，在 LPS 治疗后，这些 AM 中裂解的 caspase-3 和促炎细胞因子白细胞介素 (IL)-1β、IL-6 和肿瘤坏死因子-α 的水平增加。此外，我们证明，在矽肺小鼠模型中，LPS 暴露会加剧 AMs 中的细胞凋亡和炎症因子的释放，最终促进了肺纤维化。这些结果表明，暴露于 LPS 可能通过增加 AM 的细胞凋亡和炎症来加速矽肺肺纤维化的进展。