Evidence regarding the impact of air pollution on acute respiratory distress syndrome (ARDS) is limited, and most studies focus on ARDS onset. Our study aimed to evaluate whether exposure to fine particulate matter interferes with lung recovery and remodeling in a murine model of acute lung injury. Forty-eight mice received nebulized LPS or the vehicle (controls). Blood, BALF, lungs and spleen were collected after 5 weeks of exposure to either PM_2.5 (PM and LPS + PM group) or filtered air (control and LPS5w groups). Inflammatory cells and cytokines were assessed in the blood, BALF, lungs and spleen. Stereological analyses and remodeling assessments were performed by histology. The LPS + PM group showed increased BALF leukocytes, characterized by increased macrophages, increased IL-1β and IL-6 levels, anemia and thrombocytopenia. Moreover, we also observed septal thickening, decreased alveolar air space total volume and, septa surface density. Finally, regarding tissue remodeling, we observed elastosis of the lung parenchyma, and unlike in the LPS5w group, we did not observe fibrosis in the LPS + PM group. In conclusion, the delayed inflammation resolution due to subchronic exposure to PM_2.5 could be influenced by low systemic and local lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.

关于空气污染对急性呼吸窘迫综合征 (ARDS) 影响的证据有限，大多数研究都集中在 ARDS 发病上。我们的研究旨在评估暴露于细颗粒物是否会干扰急性肺损伤小鼠模型中的肺恢复和重塑。四十八只小鼠接受雾化的 LPS 或载体（对照）。暴露于 PM _2.5 5 周后收集血液、BALF、肺和脾脏（PM 和 LPS + PM 组）或过滤空气（控制和 LPS5w 组）。在血液、BALF、肺和脾中评估炎症细胞和细胞因子。通过组织学进行体视学分析和重塑评估。LPS+PM组BALF白细胞增多，表现为巨噬细胞增多，IL-1β和IL-6水平升高，贫血和血小板减少。此外，我们还观察到间隔增厚、肺泡空气空间总体积和间隔表面密度降低。最后，关于组织重塑，我们观察到肺实质的弹性组织增生，与 LPS5w 组不同，我们没有在 LPS + PM 组中观察到纤维化。总之，亚慢性暴露于 PM _2.5导致炎症消退延迟 可能受到全身和局部淋巴细胞计数低的影响，导致肺损伤恢复和组织重塑受损。