Particulate Matter-Induced Airway Hyperresponsiveness Is Lymphocyte Dependent

Details

• Personal Author:
  Breysse P ; Clark J ; Davila M ; Saunders V ; Sproles A ; Wills-Karp M
• Description:
  Background: Exposure to airborne particulate matter (PM), a major component of air pollution, has been associated with increases in both exacerbations of and hospitalizations for asthma. We have previously shown that exposure to ambient PM 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 remains unknown. Objective: We investigated whether T lymphocytes play a role in AUB-induced AHR. Methods: We compared the effects of AUB exposure on the allergic phenotype in wild-type (WT) BALB/c mice and in mice deficient in recombinase-activating gene-1 (Rag1-/-) that lack mature lymphocytes. Results: We found that exposure of WT mice to AUB induced AHR concomitant with increases in the numbers of bronchoalveolar lavage (BAL) fluid lymphocytes, eosinophils, neutrophils, and mucus-containing cells in the lungs of WT mice. Interestingly, we show for the first time that these effects were associated with significant elevations in interleukin (IL)-17A, IL-17F, and T-helper 2 cell (TH2) (IL-13, IL-5) cytokine levels in lung cells, as well as reductions in the levels of the suppressive cytokine IL-10. Interestingly, Rag1-/- mice failed to develop AUB-induced AHR; however, AUB-induced BAL fluid 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. [Description provided by NIOSH]
• Subjects:
  Air Pollutants, Occupational Air Pollution Animals Asthma Asthma, Occupational Immune System Occupational Health Particulate Matter Respiratory System Safety
• Keywords:
  Airborne Particulates Air Pollution Animal Studies Author Keywords: Asthma Immune Reaction Interleukins Outdoor Air Particulate Matter Particulates Pulmonary Respiratory Irritants

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• ISSN:
  0091-6765
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Journal Article
• Place as Subject:
  Maryland ; Ohio ; OSHA Region 3 ; OSHA Region 5
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  118
• Issue:
  5
• NIOSHTIC Number:
  nn:20062751
• Citation:
  Environ Health Perspect 2010 May; 118(5):640-646
• Contact Point Address:
  M. Wills-Karp, Division of Immunobiology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave., MLC 7038, Cincinnati, OH 45229 USA
• Email:
  wildc7@cchmc.org
• Federal Fiscal Year:
  2010
• Performing Organization:
  Johns Hopkins University
• Peer Reviewed:
  True
• Start Date:
  20050701
• Source Full Name:
  Environmental Health Perspectives
• End Date:
  20280630
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:552ef638e8b055f9caec6aa41bf632bf54a0f4ac1e422efc8e6ce3e3704239e1fc9e98f9915f5f56a54cdaa970a781c7ea089709052c8663b6c15bcfbff49e1b
• Download URL:
  https://stacks.cdc.gov/view/cdc/225941/cdc_225941_DS1.pdf
• File Type:
  [PDF - 2.69 MB ]