Related Experiment Video
Updated: Mar 19, 2026
Assessment of Respiratory Function in Conscious Mice by Double-chamber Plethysmography
Published on: July 10, 2018
PM2.5-induced airway inflammation and hyperresponsiveness in NC/Nga mice
Keiki Ogino1, Kenjiro Nagaoka1, Tomoaki Okuda2
1Department of Public Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan.
Abstract:
The allergic inflammatory effects of particulate matter (PM) 2.5, collected with the cyclone system in Yokohama city in Japan, were investigated in NC/Nga mice, which are hypersensitive to mite allergens. PM2.5 with alum was injected intraperitoneally for sensitization. Five days later, 200 μg of PM2.5 in 25 μL of saline was administered to mice intranasally five times for further sensitization. On the 11th day, PM2.5 was administered as a challenge. On the 12th day, mice were examined for airway hyperresponsiveness (AHR), the bronchoalveolar lavage fluid (BALF) cell count, mRNA expression of Th1 , Th2 cytokines, and metallothioneins in lung tissue, and histopathology. PM2.5 increased AHR, total cell numbers including eosinophils in BALF, and mRNA levels of IL-5, IL-22, eotaxin, eotaxin 2, and metallothionein 3. In PM2.5-induced lungs, inflammation was observed around the bronchus. These results demonstrate that PM2.5 alone, collected with the cyclone system in Yokohama city in Japan, induces asthma-like airway inflammation. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1047-1054, 2017.
Insights
Particulate matter (PM) 2.5 collected in Yokohama, Japan, triggers asthma-like airway inflammation in mice. Exposure increased airway hyperresponsiveness and inflammatory markers, indicating PM2.5 as a potential asthma exacerbator.
Area of Science:
- Environmental Toxicology
- Immunology
- Respiratory Medicine
Background:
- Particulate matter (PM) 2.5 is a component of air pollution linked to respiratory issues.
- NC/Nga mice are a validated model for studying allergic inflammation due to their hypersensitivity to allergens.
Purpose of the Study:
- To investigate the allergic inflammatory effects of PM2.5 collected in Yokohama, Japan.
- To determine if PM2.5 alone can induce asthma-like symptoms and inflammation in a sensitive mouse model.
Main Methods:
- NC/Nga mice were sensitized with PM2.5 and alum, followed by intranasal PM2.5 administration.
- Assessments included airway hyperresponsiveness (AHR), bronchoalveolar lavage fluid (BALF) cell counts, cytokine mRNA expression (Th1/Th2), and lung histopathology.
Main Results:
- PM2.5 exposure significantly increased AHR and eosinophil counts in BALF.
- Elevated mRNA levels of IL-5, IL-22, eotaxin, eotaxin 2, and metallothionein 3 were observed.
- Histopathology revealed inflammation around the bronchi in PM2.5-exposed lungs.
Conclusions:
- PM2.5 collected in Yokohama induces asthma-like airway inflammation in NC/Nga mice.
- These findings highlight the potential of PM2.5 as a standalone agent in exacerbating allergic airway diseases.
