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Allergy, Asthma & Clinical Immunology

Open Access

Co-exposure to allergen and diesel exhaust enhance inflammatory responses in human airway submucosa

  • Ali Hosseini1, 2Email author,
  • Tillie L Hackett2,
  • Jeremy Hirota1, 2,
  • Kelly McNagny3 and
  • Chris Carlsten1, 2
Allergy, Asthma & Clinical Immunology201410(Suppl 2):A57

Published: 18 December 2014


TryptaseDiesel ExhaustEosinophil Cationic ProteinActivate Mast CellMite Allergen


Asthma is a chronic condition described by inflammation of the airways and lungs. Diesel exhaust (DE) is a major contributor to ambient particulate matter (PM) air pollution. There is rising evidence that PM acts as adjuvant on the immune responses and may lead to augmentation of allergic inflammation [1, 2]. We aim to elucidate if DE increases allergen-induced inflammation and cellular immune response in the airways of atopic human subjects.


15 volunteer participants with allergy to house dust mite allergen (Der p 1), birch or Timothy grass were recruited. In a randomized fashion, subjects inhaled DE (300µg PM2.5/m3) or filtered air for 120 minutes. One hour following the exposure, the extract of an aeroallergen to which the individual is sensitive, or placebo (sterile saline), was instilled into contralateral lung segments through bronchoscopy. Endobronchial biopsies from these same segments were then acquired 48 hours after each exposure. This was repeated 4 weeks later in each subject with the alternative inhalant. Thus, biopsies under 4 different conditions were created: filtered air + saline (FAS), DE + saline (DES), filtered air + allergen (FAA) and DE + allergen (DEA). Biopsies were processed and embedded in glycol methanlacrylate acrylic resin and serial sections were cut to 2µm and used for immunostaining with monoclonal antibodies to tryptase and eosinophil cationic protein (ECP). The percent positivity and distribution of activated mast cells (tryptase+) and eosinophils (ECP+) were quantified in the bronchial submucosa by Aperio ImageScope software.


The percent positivity for tryptase expression: FAS=0.54±0.05, DES=0.51±0.18, FAA=0.63±0.24, DEA= 0.94±0.23. The percent positivity for ECP expression: FAS=0.35±0.17, DES=0.38±0.11, FAA=0.61±0.14, DEA=0.73±0.33. Data are presented as mean ± SEM (n=6).


Our preliminary data suggest that DE may enhance the inflammatory response to allergen in atopic individuals. This data is novel in the context of human lung tissue.



This study is funded by the Canadian Institutes of Health Research (CIHR). A.H. is supported by CIHR Transplantation Scholarship Training Program.

Authors’ Affiliations

Department of Medicine, University of British Columbia, Vancouver, Canada
University of British Columbia, James Hogg Research Centre of the Heart + Lung Institute, Vancouver, Canada
University of British Columbia, Biomedical Research Centre, Vancouver, Canada


  1. Riedl M, Diaz-Sanchez D: Biology of diesel exhaust effects on respiratory function. Journal of Allergy and Clinical Immunology. 2005, 115 (2): 221-228. 10.1016/j.jaci.2004.11.047.View ArticlePubMedGoogle Scholar
  2. Nel AE, Diaz-Sanchez D, Ng D, Hiura T, Saxon A: Enhancement of allergic inflammation by the interaction between diesel exhaust particles and the immune system. Journal of Allergy and Clinical Immunology. 1998, 102 (4): 539-554. 10.1016/S0091-6749(98)70269-6.View ArticlePubMedGoogle Scholar


© Hosseini et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.