The influence of PM2.5 on lung injury and cytokines in mice

Abstract

Exposure to particulate matter ≤2.5 µm in diameter (PM2.5) profoundly affects human health. However, the role of PM2.5 on lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PM2.5 pollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NOx and PM2.5 were significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PM2.5 in macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PM2.5 pollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PM2.5 can activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage.

Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?

“…Air pollution represents one of the most well-known causes of prolonged inflammation, eventually leading to an innate immune system hyper-activation. In a small cohort of mice exposed for three months to particulate matter 2.5 mm in diameter (PM 2.5 ), IL-4, TNF-a and transforming growth factor (TGF)-b1 were significantly increased in both serum and lung parenchyma, as well as leucocytes and macrophages (Yang et al, 2019). Obviously, a high systemic inflammation impairs heart function too, as witnessed in another cohort of mice exposed to PM 2.5 and PM 10 (Radan et al, 2019).…”

Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis

“…PM2.5 mainly contains 16 kinds of polycyclic aromatic hydrocarbons (PAHs) and metals, and excessive production of ROS is one of the key factors for PM2.5-induced cell damage. Our previous studies have shown that PM2.5 aggravates allergic asthma in mice by promoting inflammatory responses and inhibiting autophagy 39 . At the same time, we also found that PM2.5 promotes apoptosis and autophagy in alveolar epithelial cells through ROS/AMPK signaling 8 .…”

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content

“…In our study too, long-term exposure to PM 2.5 was associated with high systemic inflammation markers (CRP and LDH) and low FEV 1 % and D LCO among study populations. PM 2.5 and UFP induced inflammation at the alveolar epithelium level [26,27]. D LCO measurement is based on exchanged oxygen from the lungs into the blood at the level of the alveolar membrane and vascular endothelium.…”