PM2.5 and water-soluble components induce airway fibrosis through TGF-β1/Smad3 signaling pathway in asthmatic rats

Rosa laevigata Attenuates Allergic Asthma Exacerbated by Water-Soluble PM by Downregulating the MAPK Pathway

“…The metal smelting process has recently been reported as the most important emission source of PM, as it increases the inclusion of various heavy metals in high concentrations in fine dust ( Zhang H. et al, 2013 ; Ogundele et al, 2017 ; Zhang et al, 2018 ). Recently, studies comparing the different pathological effects of insoluble and soluble PM extracts have been actively conducted to investigate the potential contribution of various components of PM to respiratory diseases ( Velali et al, 2016b ; Jeong et al, 2017 ; Zhao et al, 2019a ; Zhao et al, 2020a ; Wu et al, 2021a ). Among these, WPM contains abundant contaminants with significant heavy metal and inorganic ion content.…”

“…In addition, it contains heavy metals harmful to the human body, such as Pb, As, Cd. Repeated exposure to WPM containing these heavy metals in the nasal cavities of asthmatic mice can cause allergic asthma characterized by eosinophilic and neutrophil infiltration due to pro-inflammatory cell reactions and Th2 cell immune pathway-related inflammatory reactions ( Zhao et al, 2019a ; Zhao et al, 2020a ; Wu et al, 2021a ). The histological findings of this study shown through H&E staining similarly showed that the airway epithelium was thicker in mice induced with OVA + WPM than in mice induced with asthma only by OVA, which proves that many inflammatory cells were mobilized to the bronchioles.…”

“…In addition, WPM promotes the expression of pro-inflammatory cytokines and chemokines by activating the NF-kB and MAPK pathways, which are closely related to multiple inflammatory responses, and aggravates the onset of allergic asthma by enhancing the infiltration of inflammatory cells in the lungs ( Zhao et al, 2020b ). There is also abundant evidence supporting an association between WPM and asthma, including that WPM induces pulmonary fibrosis via TGF-β1/Smad3 signaling in a murine model of asthma ( Wu et al, 2021b ). Therefore, as interest in the worsening of respiratory health due to PM increases, many researchers around the world are trying to discover treatments for various respiratory diseases that are aggravated by PM, such as asthma and COPD.…”

Effects of indoor air pollution on clinical outcomes in patients with interstitial lung disease: protocol of a multicentre prospective observational study

“…PM 2.5 is small enough to penetrate deeply into the lung parenchyma, leading to various harmful effects such as increased reactive oxygen stress, release of inflammatory cytokines and activation of inflammatory cells 16. In both in vitro and in vivo models, PM 2.5 exposure has been shown to promote the development of pulmonary fibrosis 17–19. Specifically, chronic exposure of human bronchial epithelial cells to PM 2.5 results in the activation of the transforming growth factor-beta 1 (TGF-β1)/SMAD3 pathway, TGF-β1 excretion and epithelial–mesenchymal transition,18 which are known to promote the proliferation and activation of fibroblast.…”

Ligustilide attenuates airway remodeling in COPD mice by covalently binding to MH2 domain of Smad3 in pulmonary epithelium, disrupting the Smad3‐SARA interaction

“…The TGF‐β1/Smad3 signaling pathway is implicated in the development and progression of airway remodeling (Roberts et al, 2006; Wu et al, 2021). Smad3, an indispensable transcriptional modulator in this pathway, is recruited to the TGF‐β1 receptor by Smad anchor for receptor activation (SARA) for phosphorylation, forming complexes with Smad4.…”