Abstract
Particulate matter (PM) air pollution has been associated with an increase in the incidence of chronic allergic diseases; however, the mechanisms underlying the effect of exposure to natural ambient air pollution in chronic allergic diseases have not been fully elucidated. In the present study, we aimed to investigate the cellular responses induced by exposure to natural ambient air pollution, employing a mouse model of chronic allergy. The results indicated that exposure to ambient air pollution significantly increased the number of eosinophils in the nasal mucosa. The modulation of gene expression profile identified a set of regulated genes, and the Triggering Receptor Expressed on Myeloid cells1(TREM1) signaling canonical pathway was increased after exposure to ambient air pollution. In vitro, PM2.5 increased Nucleotide-binding oligomerization domain-containing protein 1 (Nod1) and nuclear factor (NF)-κB signaling pathway activation in A549 and HEK293 cell cultures. These results suggest a novel mechanism by which, PM2.5 in ambient air pollution may stimulate the innate immune system through the PM2.5-Nod1-NF-κB axis in chronic allergic disease.
Highlights
Environmental pollution is a major problem in China, especially Beijing; with increased number of vehicles, heating in the winter season, and industrial emissions being major contributors to airborne particulate matter (PM)
By using the Nucleotide-binding oligomerization domain-containing protein 1 (Nod1)-Flag and nuclear factor (NF)-κB-dependent green fluorescent protein (GFP) reporter bioassay established by Hasegawa et al17. for screening and characterizing Nod1-stimulatory activities in HEK293-Nod1-GFP cells, we found that PM2.5 + pollen (2.13 ± 0.52) significantly increased the level of Nod1-stimulatory activities in these cells, compared to untreated cells [Fig. 5B]
We applied a novel approach for investigating the underlying mechanism of cell response to air pollution exposure, by establishing a chronic allergy mouse model and exposing this to the real environment, when the concentrations of PM2.5 are known to be high from September to March in Beijing
Summary
Environmental pollution is a major problem in China, especially Beijing; with increased number of vehicles, heating in the winter season, and industrial emissions being major contributors to airborne particulate matter (PM). Modulation of gene expression has been shown to play a major role in the activation of toxic pathways, and in this regard gene signatures have the potential to act as biomarkers of PM2.5 exposure. Chu and colleagues[10] have recently demonstrated that several genes and gene networks; many of which have been implicated in ischemic heart disease, chronic obstructive pulmonary disease (COPD), lung cancer, and other pollution-related illnesses; were differentially www.nature.com/scientificreports/. Exposure to Milan PM2.5 has been shown to alter gene expression and the production of reactive oxygen species (ROS) in human alveolar epithelia cells (A549), and suggested that DNA damage was likely to be related to changes in the cytochrome P450 (CYP) enzyme activity[11]. A more recent study has demonstrated sex-specific candidate gene expression in response to PM10 exposure in humans[13]. PM2.5 exposure induced the intracellular pattern recognition receptor Nod[1] activity and stimulated an immune reaction by the activation of NF-κB signaling pathway
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