Changes in gene expression in chronic allergy mouse model exposed to natural environmental PM2.5-rich ambient air pollution

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.

Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)–nucleotide‐binding, oligomerization domain–like receptor family, pyrin domain containing 3 (NLRP3)–caspase‐1–interleukin 1β (IL‐1β) pathway

“…creased AR mobidity. 2 Indeed, recent studies from China have demonstrated that the concentrations of particulate matter <2.5 μm (PM2.5) and PM10 in the air were closely related to the incidence of AR, 3,4 and additionally significantly impacted the type and concentration of pollen. 5 Evidence indicates that nasal epithelial cells play an integral role in innate and adaptive immune responses to diverse environmental pollutants and allergens by synthesizing and releasing numerous inflammatory cytokines.…”

“…The prevalence of AR has markedly increased during the past 30 years, especially in developing countries, with increasing evidence showing that air pollution is likely to be associated with increased AR mobidity 2 . Indeed, recent studies from China have demonstrated that the concentrations of particulate matter <2.5 µm (PM2.5) and PM10 in the air were closely related to the incidence of AR, 3,4 and additionally significantly impacted the type and concentration of pollen 5 …”

Effects of Environmental PM_2.5 on Adult SD Rat Lung Transcriptional Profile

“…Furthermore, excessive ROS in the lung tissue would activate neutrophils, which resulted in continuous airway inflammatory reactions. Studies indicated that PM 2.5 would cause cell infiltration and structural remodeling [20]. And in this study, we observed the cells response to amyloid-beta after PM 2.5 exposure, which was reported to promote fiber deposition [47].…”

“…Several studies have suggested that the alternation of gene expression played a major role in the activation of pathways induced by toxicant exposure [20][21][22][23][24]. Recent studies indicated that PM 2.5 could enter cells via pinocytosis, and could alter the gene expression of lung epithelial and myocardial cells.…”

The Influence of Air Pollution on the Development of Allergic Inflammation in the Airways in Krakow’s Atopic and Non-Atopic Residents

“…For ethical reasons, it is impossible to perform in vivo provocations with PM in humans, and most studies on its mechanism of action are performed in mice [10]. The basophil activation test (BAT) is an in vitro specific provocation test, which can replace potentially dangerous in vivo provocations [11].…”