Air pollution impairs recovery and tissue remodeling in a murine model of acute lung injury

• Published in: Scientific reports Vol. 10; no. 1; p. 15314
• Main Authors: de Souza Xavier Costa, Natália, Ribeiro Júnior, Gabriel, dos Santos Alemany, Adair Aparecida, Belotti, Luciano, Schalch, Alexandre Santos, Cavalcante, Marcela Frota, Ribeiro, Susan, Veras, Mariana Matera, Kallás, Esper Georges, Saldiva, Paulo Hilário Nascimento, Dolhnikoff, Marisa, Ferraz da Silva, Luiz Fernando
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 17.09.2020
• Subjects: 631/1647/767/1424; 631/250/256/2516; 631/443/1784; Acute Lung Injury - metabolism; Acute Lung Injury - pathology; Air Pollution - adverse effects; Animals; Bronchoalveolar Lavage Fluid; Cytokines - metabolism; Disease Models, Animal; Humanities and Social Sciences; Inflammation - metabolism; Inflammation - pathology; Interleukin-1beta - metabolism; Interleukin-6 - metabolism; Lung - metabolism; Lung - pathology; Male; Mice; Mice, Inbred BALB C; multidisciplinary; Particulate Matter - adverse effects; Respiratory Distress Syndrome - metabolism; Respiratory Distress Syndrome - pathology; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-020-72130-3

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.