Korean J Asthma Allergy Clin Immunol.
2006 Mar;26(1):70-77.
Effects of Diesel Exhaust Particles on Airway Responsiveness and Remodeling in a Murine Asthma Model
Abstract
- BACKGROUND
Epidemiologic and clinical investigations have suggested a strong link between particulate air pollution and asthma. The purpose of this study was to evaluate an effects of air pollutants on a murine asthma model, focusing on diesel exhaust particles (DEP).
METHOD: The Balb/c mice were sensitized intra-peritoneally (i.p.) with ovalbumin (OVA) at days 0 and 14 and challenged intranasally with OVA at days 21, 22, and 23 (group I). The Balb/c mice were sensitized i.p. with OVA at day 0, 14 and challenged with 6 mg/10 mL of DEP at days 21, 22, and 23 (group II). Group III were sensitized with OVA at days 0 and 14, together with 0.6 mg/50 u
L of DEP every other day for 14 days and challenged with 150 ug /100 uL OVA and 6 mg/10 mL of DEP at day 21, 22, and 23. Saline sensitized-challenged mice were served as sham control. The mice were subjected to whole-body plethysmo-graphy and then killed for bronchoalveolar lavage and histology. Cytokines were measured by ELISA. Expression of goblet cell hyperplasia and smooth muscle hyperplasia in the lung tissue was detected by immunohistochemical staining.
RESULT: DEP and OVA sensitized-challenge group had a significant increase in methacholine-induced AHR, compared to sham group and group I. The levels of IL-4, IL-5, and IFN-gamma tended to increase in the BAL fluid in group III. Goblet cell hyperplasia and smooth muscle hypertrophy were more observed in group III than those in sham group, groups I and II.
CONCLUSION
This study demonstrates that DEP may aggravate airway responsiveness and remodeling in a mouse asthma model.