Ambient urban Baltimore particulate-induced airway hyperresponsiveness andinflammation in mice

Citation
Dm. Walters et al., Ambient urban Baltimore particulate-induced airway hyperresponsiveness andinflammation in mice, AM J R CRIT, 164(8), 2001, pp. 1438-1443
Citations number
24
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
164
Issue
8
Year of publication
2001
Pages
1438 - 1443
Database
ISI
SICI code
1073-449X(20011015)164:8<1438:AUBPAH>2.0.ZU;2-0
Abstract
Airborne particulate matter (PM) is hypothesized. to play a role in increas es in asthma prevalence, although a causal relationship has yet to be estab lished. To investigate the effects of real-world PM exposure on airway reac tivity (AHR) and bronchoalveolar lavage (BAL) cellularity, we exposed naive mice to a single dose (0.5 mg/ mouse) of ambient PM, coal fly ash, or dies el PM. We found that ambient PM exposure induced increases in AHR and BAL c ellularity, whereas diesel PM induced significant increases in BAL cellular ity, but not AHR. On the other hand, coal fly ash exposure did not elicit s ignificant changes in either of these parameters. We further examined ambie nt PM-induced temporal changes in AHR, BAL cells, and lung cytakine levels over a 2-wk period. Ambient PM-induced AHR was sustained over 7 d. The incr ease in AHR was preceded by dramatic increases in BAL eosinophils, whereas a decline in AHR was associated with increases. in macrophages. A Th2 cytok ine pattern (IL-5, IL-13, eotaxin) was observed early on with a shift towar d a Th1 pattern (IFN-gamma). In additional studies, we found that the activ e component(s) of ambient PM are not water-soluble and that ambient PM-indu ced AHR and inflammation are dose-dependent. We conclude that ambient PM ca n induce asthmalike parameters in naive mice, suggesting that PM exposure m ay be an important factor in increases in asthma prevalence.