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

Abstract

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 PM2.5 (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 PM2.5 could be influenced by low systemic and local lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.

LPS Response Is Impaired by Urban Fine Particulate Matter

“…The organic compounds present in the PM 2.5 , such as pollen, fungal spores, mold, and microbial components (including LPS) also play an important role in inflammation modulation [ 6 ] and, we have confirmed the presence of LPS in the PM 2.5 that the animals were exposed [ 19 ]. Nomura et al [ 35 ] showed that macrophages exposed to low levels of LPS show reduced response to a second stimulation with LPS by downregulating TLR4 leading to a time- and dose-dependent reduction in the production of inflammatory cytokines.…”

“…Lopes et al [ 17 ] reported the concentration of PM 2.5 , its black carbon (BC), and metal trace content from the collected filters. Yoshizaki et al [ 18 ] reported the polycyclic aromatic hydrocarbon content, and Costa et al [ 19 ] reported the endotoxin content.…”

Pathogenic Mechanisms of Secondary Organic Aerosols

“…Cell culture studies and animal experimental models support this assumption. Furthermore, a recent series of reported works show the deleterious effect of PM2.5, hence SOA, knowing it represents a major part of PM2.5. ,− Among these effects are septal thickening leading to a decrease of lung capacity and development of fibrotic tissues due to the massive recruitment of macrophages/monocytes and release of their protease arsenal involved in tissue remodeling , which may induce fibrosis. , Based on the literature, although scanty, the impact of SOA on lung tissues seems to translate in different pathologies. In a mouse model, we provided compelling evidence that exposure to nanoparticles led to granuloma formation in lungs .…”

Effects of air pollution on myopia: an update on clinical evidence and biological mechanisms

“…Differential regulation of microRNAs involved in oxidative stress and inflammatory processes may have contributed to arteriolar narrowing and venular widening. Animals exposed to different types of particles exhibit thickening of alveolar walls, neutrophil recruitment, and macrophage activation, thus increasing systemic oxidative stress and inflammation response, as well as stimulating the generation of ROS and pro-inflammatory cytokines, which finally enter circulation (de Souza Xavier Costa et al 2020 ). The substances involved in these systemic reactions may take some time to affect the reactivity of retinal blood vessels, even several hours after exposure, according to Louwies et al ( 2013 ).…”