Airway inflammatory responses to diesel exhaust in allergic rhinitics
Airway inflammatory responses to diesel exhaust in allergic rhinitics
CONTEXT: Proximity to traffic, particularly to diesel-powered vehicles, has been associated with inducing and enhancing allergies. To investigate the basis for this association, we performed controlled exposures of allergic rhinitics to diesel exhaust (DE) at a dose known to be pro-inflammatory in healthy individuals.
OBJECTIVE: We hypothesized that diesel-exhaust exposure would augment lower airway inflammation in allergic rhinitics.
MATERIALS AND METHODS: Fourteen allergic rhinitics were exposed in a double-blinded, randomized trial to DE (100??g/m³ PM??) and filtered air for 2?h on separate occasions. Bronchoscopy with endobronchial mucosal biopsies and airway lavage was performed 18?h post-exposure, and inflammatory markers were assessed.
RESULTS: No evidence of neutrophilic airway inflammation was observed post-diesel, however, a small increase in myeloperoxidase was found in bronchoalveolar lavage (p?=?0.032). We found no increases in allergic inflammatory cells. Reduced mast cell immunoreactivity for tryptase was observed in the epithelium (p?=?0.013) parallel to a small decrease in bronchial wash stem cell factor (p?=?0.033).
DISCUSSION AND CONCLUSION: DE, at a dose previously shown to cause neutrophilic inflammation in healthy individuals, induced no neutrophilic inflammation in the lower airways of allergic rhinitics, consistent with previous reports in asthmatics. Although there was no increase in allergic inflammatory cell numbers, the reduction in tryptase in the epithelium may indicate mast cell degranulation. However, this occurred in the absence of allergic symptoms. These data do not provide a simplistic explanation of the sensitivity in rhinitics to traffic-related air pollution. The role of mast cells requires further investigation.
160-167
Larsson, Nirina
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Brown, Joanna
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Stenfors, Nikolai
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Wilson, Susan
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Mudway, Ian S.
a9f9b1a8-2a5b-4b1f-836d-8649d3621522
Pourazar, Jamshid
d41db41e-cb53-4399-8c77-aaed8ff153a6
Behndig, Annelie F.
8b7190cd-e3ed-42a0-bc5c-8ae83c402097
February 2013
Larsson, Nirina
cd94cb36-35f5-4d1f-909a-bc4ca9d755c3
Brown, Joanna
32b96891-d0ee-4128-89a3-e68889e851ef
Stenfors, Nikolai
69c8966c-e8f8-40f8-b8b2-8e4f918953f0
Wilson, Susan
21c6875d-6870-441b-ae7a-603562a646b8
Mudway, Ian S.
a9f9b1a8-2a5b-4b1f-836d-8649d3621522
Pourazar, Jamshid
d41db41e-cb53-4399-8c77-aaed8ff153a6
Behndig, Annelie F.
8b7190cd-e3ed-42a0-bc5c-8ae83c402097
Larsson, Nirina, Brown, Joanna, Stenfors, Nikolai, Wilson, Susan, Mudway, Ian S., Pourazar, Jamshid and Behndig, Annelie F.
(2013)
Airway inflammatory responses to diesel exhaust in allergic rhinitics.
Inhalation Toxicology, 25 (3), .
(doi:10.3109/08958378.2013.765932).
(PMID:23421487)
Abstract
CONTEXT: Proximity to traffic, particularly to diesel-powered vehicles, has been associated with inducing and enhancing allergies. To investigate the basis for this association, we performed controlled exposures of allergic rhinitics to diesel exhaust (DE) at a dose known to be pro-inflammatory in healthy individuals.
OBJECTIVE: We hypothesized that diesel-exhaust exposure would augment lower airway inflammation in allergic rhinitics.
MATERIALS AND METHODS: Fourteen allergic rhinitics were exposed in a double-blinded, randomized trial to DE (100??g/m³ PM??) and filtered air for 2?h on separate occasions. Bronchoscopy with endobronchial mucosal biopsies and airway lavage was performed 18?h post-exposure, and inflammatory markers were assessed.
RESULTS: No evidence of neutrophilic airway inflammation was observed post-diesel, however, a small increase in myeloperoxidase was found in bronchoalveolar lavage (p?=?0.032). We found no increases in allergic inflammatory cells. Reduced mast cell immunoreactivity for tryptase was observed in the epithelium (p?=?0.013) parallel to a small decrease in bronchial wash stem cell factor (p?=?0.033).
DISCUSSION AND CONCLUSION: DE, at a dose previously shown to cause neutrophilic inflammation in healthy individuals, induced no neutrophilic inflammation in the lower airways of allergic rhinitics, consistent with previous reports in asthmatics. Although there was no increase in allergic inflammatory cell numbers, the reduction in tryptase in the epithelium may indicate mast cell degranulation. However, this occurred in the absence of allergic symptoms. These data do not provide a simplistic explanation of the sensitivity in rhinitics to traffic-related air pollution. The role of mast cells requires further investigation.
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Published date: February 2013
Organisations:
Clinical & Experimental Sciences
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Local EPrints ID: 352335
URI: http://eprints.soton.ac.uk/id/eprint/352335
ISSN: 0895-8378
PURE UUID: 703fa2e7-70cf-4506-b7f8-4684f0060c01
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Date deposited: 09 May 2013 13:39
Last modified: 14 Mar 2024 13:51
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Author:
Nirina Larsson
Author:
Joanna Brown
Author:
Nikolai Stenfors
Author:
Ian S. Mudway
Author:
Jamshid Pourazar
Author:
Annelie F. Behndig
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