Related Experiment Video
Updated: Jun 20, 2026
Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
Pulmonary effects of inhaled diesel exhaust in aged mice
Vasanthi R Sunil1, Kinal J Patel, Gediminas Mainelis
1Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, 160 Frelinghuysen Road, Piscataway, NJ 08854, USA. sunilvr@eohsi.rutgers.edu
Abstract:
Pulmonary morbidity and mortality resulting from exposure to fine particulate matter (PM) increases with age. The present studies analyzed potential mechanisms underlying increased susceptibility of the elderly to PM using diesel exhaust (DE) as a model. Mice (2 m and 18 m) were exposed to DE (0, 300, and 1000 microg/m(3)) for 3 h once (single) or 3 h/day for 3 days (repeated). Bronchoalveolar lavage fluid (BAL), serum and lung tissue were collected 0 and 24 h later. Exposure to DE resulted in structural alterations in the lungs of older but not younger mice, including patchy thickening of the alveolar septa and inflammatory cell localization in alveolar spaces. These effects were most pronounced 24 h after a single exposure to the higher dose of DE. Significant increases in BAL nitrogen oxides were also noted in older mice, as well as expression of lipocalin 24p3, an oxidative stress marker in the lung with no effects in younger mice. Following DE inhalation, expression of Tumor Necrosis Factor alpha (TNFalpha) was upregulated in lungs of both younger and older mice; however, this was attenuated in older animals. Whereas exposure to DE resulted in increases in lung Interleukin-6 (IL-6) expression in both older and younger mice, IL-8 increased only in older animals. In younger mice, constitutive expression of manganese superoxide dismutase (MnSOD) decreased after DE exposure, while in older mice, constitutive MnSOD was not detectable and DE had no effect on expression of this antioxidant. Taken together, these results suggest that altered generation of inflammatory mediators and MnSOD may contribute to increased susceptibility of older mice to inhaled DE.
Insights
Older mice show increased lung damage and inflammation after diesel exhaust exposure compared to younger mice, suggesting age-related susceptibility to particulate matter air pollution.
Area of Science:
- Environmental Health
- Toxicology
- Aging Research
Background:
- Particulate matter (PM) air pollution, particularly fine PM, is linked to increased pulmonary morbidity and mortality.
- Susceptibility to PM-induced lung injury appears to increase with age, but underlying mechanisms are not fully understood.
- Diesel exhaust (DE) serves as a relevant model for studying the effects of fine PM on respiratory health.
Purpose of the Study:
- To investigate the mechanisms contributing to increased susceptibility of elderly individuals to particulate matter (PM) exposure.
- To compare the effects of diesel exhaust (DE) inhalation on lung structure, inflammation, and oxidative stress in young versus aged mice.
Main Methods:
- Young (2-month-old) and aged (18-month-old) mice were exposed to varying concentrations of diesel exhaust (DE) via inhalation.
- Exposure protocols included single high-dose and repeated lower-dose DE inhalation.
- Lung tissue, bronchoalveolar lavage fluid (BAL), and serum were collected at different time points post-exposure for analysis.
Main Results:
- Aged mice exhibited structural lung alterations (e.g., alveolar septal thickening) and inflammatory cell infiltration following DE exposure, unlike younger mice.
- Older mice showed increased levels of BAL nitrogen oxides and expression of the oxidative stress marker lipocalin 24p3.
- While both age groups showed increased Tumor Necrosis Factor alpha (TNFα) and Interleukin-6 (IL-6), older mice uniquely upregulated Interleukin-8 (IL-8) and showed no change in manganese superoxide dismutase (MnSOD) expression, unlike younger mice.
Conclusions:
- Age-related differences in the generation of inflammatory mediators and antioxidant responses (MnSOD) may underlie the heightened susceptibility of older individuals to inhaled diesel exhaust.
- These findings highlight specific molecular and cellular pathways that could be targeted to mitigate the adverse effects of air pollution in the elderly.
