Departamento de Patologia, LIM-05, Faculdade de Medicina da Universidade de São Paulo, São Paulo 01246-903, Brazil.
Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas da Universidade de São Paulo, São Paulo 05508-000, Brazil.
Int J Mol Sci. 2022 Apr 1;23(7):3913. doi: 10.3390/ijms23073913.
Fine particulate matter (PM) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM on LPS-induced lung injury onset. male mice were exposed to either filtered air or ambient fine PM in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1β, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM exposure.
细颗粒物(PM)是一种复杂的混合物,具有多种化学和物理特性,与呼吸系统和心血管疾病死亡率的增加有关。我们的研究旨在探讨暴露于浓缩 PM 对 LPS 诱导的肺损伤发作的影响。雄性小鼠在环境粒子浓缩器中暴露于过滤空气或环境细颗粒物中 5 周。然后,用雾化 LPS 诱导急性肺损伤。雾化后 24 小时,用 LPS 或生理盐水处死动物。在血液、支气管肺泡灌洗液(BALF)和肺组织中评估炎性细胞和细胞因子(IL-1β、IL-4、IL-5、IL-6、IL-10、IL-17、TNF)。此外,通过体视学方法评估肺形态。我们的结果表明,PM+LPS 组显示出损伤的组织学证据,白细胞增多,中性粒细胞和巨噬细胞增多,以及混合性炎症反应特征,KC、IL-6、IL-1β、IL-4 和 IL-17 增加。我们的分析表明,LPS 雾化和 PM 暴露之间存在相互作用,以不同的方式调节炎症反应,与 LPS 或 PM 单独暴露相比具有明显不同的反应模式。需要进一步研究来解释 PM 暴露引起的免疫调节机制。