Particulate Matter Induced Airway Hyperresponsiveness is Lymphocyte Dependent
Saunders, V; Breysse, P; Clark, J; Sproles, A; Davila, M; Wills-Karp, M
HERO ID
385876
Reference Type
Journal Article
Year
2010
Language
English
PMID
| HERO ID | 385876 |
|---|---|
| In Press | No |
| Year | 2010 |
| Title | Particulate Matter Induced Airway Hyperresponsiveness is Lymphocyte Dependent |
| Authors | Saunders, V; Breysse, P; Clark, J; Sproles, A; Davila, M; Wills-Karp, M |
| Journal | Environmental Health Perspectives |
| Volume | 118 |
| Issue | 5 |
| Page Numbers | 640-646 |
| Abstract | Background. Exposure to airborne particulate matter, which is a major component of air pollution, has been associated with increases in both exacerbations and hospitalizations for asthma. We have previously shown that exposure to ambient particulate matter collected in urban Baltimore (AUB) induces airway hyperresponsiveness (AHR), eosinophilic and neutrophilic inflammation, and the recruitment of T cells. However, the mechanism(s) by which it induces these features of asthma remain unknown. Objective. To determine whether T lymphocytes play a role in AUB-induced AHR. Methods. We compared the effects of AUB exposure on the allergic phenotype in wildtype Balb/c and recombinase-activating-gene-1 (Rag1) deficient mice lacking mature lymphocytes. Results. We found that exposure of wild-type mice to AUB induced AHR concomitant with increases in the numbers of bronchoalveolar lavage lymphocytes, eosinophils and neutrophils, and mucus containing cells in the lungs of wildtype mice. Interestingly, we show for the first time that these effects were associated with significant elevations in lung cell IL-17A and F and Th2 (IL-13, IL-5) cytokine levels and reductions in the levels of the suppressive cytokine, IL-10. Interestingly, Rag1-/- mice failed to develop AUB-induced AHR, however, AUB-induced BAL cellularity and mucus cell changes were only partially inhibited in Rag1-/- mice. Conclusions. Taken together our results suggest that AUB exposure increases the pathophysiological features of asthma via activation of lymphocyte-dependent pathways. These results provide a plausible biological mechanism for the strong association between PM exposure and the increased severity of asthma. |
| Doi | 10.1289/ehp.0901461 |
| Pmid | 20061214 |
| Wosid | WOS:000277846800028 |
| Is Certified Translation | No |
| Dupe Override | No |
| Comments | Source: Web of Science 000277846800028 |
| Is Public | Yes |
| Language Text | English |
| Keyword | asthma; interleukins; outdoor air; particulate matter; pulmonary |
| Is Qa | No |