Allergic Airway Inflammation by Nasal Inoculation of Particulate Matter (PM2.5) in NC/Nga Mice

Abstract

To evaluate the effect of airborne particulate matter 2.5 (PM2.5) in winter on airway inflammation, water-soluble supernatant (Sup) and water-insoluble precipitate (Pre) in PM2.5 were inoculated in NC/Nga mice with high sensitivity to mite allergens. Sup with aluminum oxide was injected intraperitoneally for sensitization. Five days later, Sup, Pre or both Sup and Pre were inoculated via the nasal route five times for more sensitization and a challenge inoculation on the 11th day in NC/Nga mice. On the 12th day, mice were examined for airway hyperresponsiveness (AHR), BALF cell count and IL-1β concentration, mRNA expression of Th1 and Th2 cytokines, chemokines such as eotaxin 1 and eotaxin 2, inflammasomal complex molecules such as IL-1β, caspase 1 and the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) in lung tissue as well as histopathology. The synergistic effect of Sup and Pre was observed in terms of increases in AHR, BALF cells, the mRNA expression of IL-13, eotaxin1 and IL-1β, and the IL-1β concentration in BALF. Intracellular deposits of insoluble particulates were observed in macrophages around inflammatory granulation of the mouse group treated with Sup and Pre. These results suggest that PM2.5 can induce airway hyperresponsiveness in mice with genetically high sensitivity to mite allergens by an inflammasome-associated mechanism and synergistic action of insoluble particulates and soluble components.

Association Between Environmental Particulate Matter and Carpal Tunnel Syndrome in Patients Undergoing Hemodialysis

“…Reactive inflammation in lesions in which β2-microglobulin amyloid was deposited was associated with a marked infiltration of activated macrophages expressing cytokines, such as interleukin-1, tumor necrosis factor-alpha, and transforming growth factor-beta [14]. Only animal study also showed that after oropharyngeal aspiration of PM 2.5 , robust production of IL-1 by leukocytes in the lung tissue was noted [15, 16]. Brucker et al showed that PM 2.5 was also associated with higher inflammatory markers, including IL-1β in taxi drivers with occupational exposure to air pollution [17].…”

PM2.5-induced airway inflammation and hyperresponsiveness in NC/Nga mice

“…We are the first to demonstrate that pure PM2.5 collected in Yokohama City using the cyclone system evoked allergic airway inflammation in mice. We previously reported that PM2.5 collected using a high volume air sampler and eluted from filters induced allergic airway inflammation, as represented by an increase in AHR, the number of eosinophils in BALF, and the expression of cytokines such as IL‐4, IL‐13, and IL‐1β (Ogino et al, ). In the present study, the expression of IL‐5 and IL‐22 was up‐regulated, whereas that of IL‐4, IL‐13, and IL‐1β was not.…”

Therapeutic effects of stemonine on particulate matter 2.5‑induced chronic obstructive pulmonary disease in mice

“…In addition, PM 2.5 accumulates toxic heavy metals, acid oxides, organic pollutants, bacteria and viruses in the air, PM 2.5 can also remain in the air for a long time and be deposited in the lungs through inhalation, so it is a major threat to human health (2,3). Numerous previous studies have suggested that PM 2.5 can stimulate the production of reactive oxygen species (ROS) and certain inflammatory mediators, resulting in changes to vascular permeability, airway constriction and tissue injury (4)(5)(6). The majority of previous studies investigating PM 2.5 have histopathologically examined lung sections (7,8).…”