Acute inflammatory responses to diesel exhaust and ozone in human airways
Acute inflammatory responses to diesel exhaust and ozone in human airways
Using controlled human exposures along with immunohistochemistry and RT PCR-ELISA, the studies presented in this thesis have examined the hypothesis that the adverse respiratory effects of DE and ozone in human lung are mediated by the generation of acute cellular and mediator inflammatory responses in the airways.
The study presented in Chapter 3 has demonstrated that short-term controlled exposures to DE at high ambient concentrations induced an acute inflammatory response in the airways and peripheral blood of healthy human subjects six hours post exposure. Chapter 4 investigated the hypothesis that DE induced airway inflammation is mediated by enhanced gene transcription of cytokines.
The study presented in Chapter 5 has demonstrated that exposure to 200 ppb ozone for 2 hours induced enhanced gene transcription of IL-8 in the proximal bronchial tissue as well as bronchial wash cells, and an associated trend towards a significant increase in IL-5 and TNFα mRNA gene transcripts in the bronchial tissue of atopic mild asthmatic subjects six hours post exposure. These proinflammatory cytokines play an important role in the pathogenesis of asthma and their increased gene transcription in the airways of asthmatics following short-term exposure to ozone offers a plausible underlying mechanism for ozone induced asthma exacerbations.
The study presented in Chapter 6 has demonstrated that exposure to 200 ppb ozone for 2 hours reduced mRNA gene transcript levels of IL-1β, IL-5 and GM-CSF in the proximal bronchial tissue of healthy human subjects at an earlier time point of 1.5 hours post exposure. These findings are likely due to ozone induced epithelial cell shedding from proximal bronchial tissue, or due to increased production of PGE2 by airway epithelial cells, which can downregulate gene transcription of several proinflammatory cytokines.
The study presented in Chapter 7 demonstrated that human airway epithelial cells are a cellular source of IL-5.
University of Southampton
Salvi, Sundeep Santosh
c9d2fc19-a457-41ad-be9e-ec63361232a6
1999
Salvi, Sundeep Santosh
c9d2fc19-a457-41ad-be9e-ec63361232a6
Salvi, Sundeep Santosh
(1999)
Acute inflammatory responses to diesel exhaust and ozone in human airways.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Using controlled human exposures along with immunohistochemistry and RT PCR-ELISA, the studies presented in this thesis have examined the hypothesis that the adverse respiratory effects of DE and ozone in human lung are mediated by the generation of acute cellular and mediator inflammatory responses in the airways.
The study presented in Chapter 3 has demonstrated that short-term controlled exposures to DE at high ambient concentrations induced an acute inflammatory response in the airways and peripheral blood of healthy human subjects six hours post exposure. Chapter 4 investigated the hypothesis that DE induced airway inflammation is mediated by enhanced gene transcription of cytokines.
The study presented in Chapter 5 has demonstrated that exposure to 200 ppb ozone for 2 hours induced enhanced gene transcription of IL-8 in the proximal bronchial tissue as well as bronchial wash cells, and an associated trend towards a significant increase in IL-5 and TNFα mRNA gene transcripts in the bronchial tissue of atopic mild asthmatic subjects six hours post exposure. These proinflammatory cytokines play an important role in the pathogenesis of asthma and their increased gene transcription in the airways of asthmatics following short-term exposure to ozone offers a plausible underlying mechanism for ozone induced asthma exacerbations.
The study presented in Chapter 6 has demonstrated that exposure to 200 ppb ozone for 2 hours reduced mRNA gene transcript levels of IL-1β, IL-5 and GM-CSF in the proximal bronchial tissue of healthy human subjects at an earlier time point of 1.5 hours post exposure. These findings are likely due to ozone induced epithelial cell shedding from proximal bronchial tissue, or due to increased production of PGE2 by airway epithelial cells, which can downregulate gene transcription of several proinflammatory cytokines.
The study presented in Chapter 7 demonstrated that human airway epithelial cells are a cellular source of IL-5.
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Published date: 1999
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Local EPrints ID: 463974
URI: http://eprints.soton.ac.uk/id/eprint/463974
PURE UUID: 7be5db21-5396-42ee-905c-3023ba7ef994
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Date deposited: 04 Jul 2022 20:59
Last modified: 23 Jul 2022 02:15
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Author:
Sundeep Santosh Salvi
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