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Event
Thu 9/19/2019 11:00AM - 12:00PM
EOH Journal Club
Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen EOH Journal Club
Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen
Thu 9/19/2019 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Brandy Hill

Paper: Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen. A Randomized, Double-Blind Crossover Study

Authors: Denise J. Wooding, Min Hyung Ryu, Anke Huls, Andrew D. Lee, David T. S. Lin, Christopher F. Rider, Agnes C. Y. Yuen, and Chris Carlsten

Abstract:
Rationale: Diesel exhaust (DE), an established model of trafficrelated
air pollution, contributes significantly to the global burden of
asthma and may augment the effects of allergen inhalation. Newer
diesel particulate-filtering technologies may increaseNO2 emissions,
raising questions regarding their effectiveness in reducing harm from
associated engine output.

Objectives: To assess the effects of DE and allergen coexposure on
lung function, airway responsiveness, and circulating leukocytes, and
determine whether DE particle depletion remediates these effects.

Methods: In this randomized, double-blind crossover study, 14
allergen-sensitized participants (9 with airway hyperresponsiveness)
underwent inhaled allergen challenge after 2-hour exposures to DE,
particle-depleted DE (PDDE), or filtered air. The control condition
was inhaled saline after filtered air. Blood sampling and spirometry
were performed before and up to 48 hours after exposures. Airway
responsiveness was evaluated at 24 hours.

Measurements and Main Results: PDDE plus allergen
coexposure impaired lung function more than DE plus allergen,
particularly in those genetically at risk. DE plus allergen and PDDE
plus allergen each increased airway responsiveness in normally
responsive participants.DEplus allergen increased blood neutrophils
and was associated with persistent eosinophilia at 48 hours. DE and
PDDE each increased total peripheral leukocyte counts in a manner
affected by participant genotypes. Changes in peripheral leukocytes
correlated with lung function decline.

Conclusions: Coexposure to DE and allergen impaired lung
function, which was worse after particle depletion (which increased
NO2). Thus, particulates are not necessarily the sole or main
culprit responsible for all harmful effects of DE. Policies and
technologies aimed at protecting public health should be scrutinized
in that regard.
Clinical trial registered with www.clinicaltrials.gov (NCT02017431).

Keywords: diesel exhaust; asthma; filter; genetic susceptibility


4140 Public Health, Young Seminar Room

Recent Events

EOH Journal Club

EOH Journal Club - Spring 2017 - Heng Bai

Thursday 3/23 11:00AM - 12:00PM
EOH Journal Club Seminar - Spring 2017

Date: Thursday March 23, 2017
Time: 11am - 12pm
Presenter: Heng Bai

Paper: 
In vivo activation of a T helper 2-driven innate immune response in
lung fibrosis induced by multi-walled carbon nanotubes

Authors: Dong J, Ma Q

Abstract:
Pulmonary exposure to certain forms of carbon nanotubes (CNT) induces
fibrosing lesions in the lungs that manifest an acute inflammation
followed by chronic interstitial fibrosis. The mechanism of CNT-induced
fibrogenesis is largely unknown. The biphasic development with
drastically distinct pathologic manifestations suggests a junction of
acute-to-chronic transition. Here we analyzed the molecular pathways and
regulators underlying the pathologic development of CNT-induced lung
fibrosis. Mice were exposed to multi-walled CNT (MWCNT; XNRI MWNT-7,
Mitsui; 40 μg) by pharyngeal aspiration for 7 days along with vehicle
and carbonaceous controls. Genome-wide microarray analyses of the lungs
identified a range of differentially expressed genes that potentially
function in the acute-to-chronic transition through pathways involving
immune and inflammatory regulation, responses to stress and
extracellular stimuli, and cell migration and adhesion. In particular, a
T helper 2 (Th2)-driven innate immune response was significantly
enriched. We then demonstrated that MWCNT induced the expression of Th2
cytokines interleukin (IL)-4 and IL-13, and a panel of signature
downstream genes, such as Il4i1, Chia, and Ccl11/Eotaxin, time
dependently. Induction of Th2 cytokines took place in CD4+ T lymphocytes
indicating activation of Th2 cells. Furthermore, induction involved
activation of a Th2 cell-specific signaling pathway through
phosphorylation of STAT6 and up-regulation of GATA-3 to mediate the
transcription of Th2 target genes. Our study uncovers activation of a
Th2-driven immune/inflammatory response during pulmonary fibrosis
development induced by MWCNT. The findings provide novel insights into
the molecular events that control the transition from an acute
inflammatory response to chronic fibrosis through Th2 functions in
CNT-exposed lungs



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Last Updated On Friday, February 24, 2017 by Orbell, Adam W
Created On Friday, February 24, 2017

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