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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

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EOH Journal Club

EOH Journal Club - Fall 2017 - Shawn Ting

Thursday 11/2 11:00AM - 12:00PM
EOH Journal Club Seminar - Fall 2017

Date: Thursday November 2, 2017

Time: 11am - 12pm

Presenter: Shawn/Hsiu-Chi Ting

Paper:  PEBP1 Wardens Ferroptosis by Enabling Lipoxygenase Generation of Lipid Death Signals

Authors: Sally E. Wenzel, Yulia Y. Tyurina, Jinming Zhao, ..., Ivet Bahar, Hulya Bayır, Valerian E. Kagan

Abstract: Ferroptosis is a form of programmed cell death that
is pathogenic to several acute and chronic diseases
and executed via oxygenation of polyunsaturated
phosphatidylethanolamines (PE) by 15-lipoxygenases
(15-LO) that normally use free polyunsaturated
fatty acids as substrates. Mechanisms
of the altered 15-LO substrate specificity are enigmatic.
We sought a common ferroptosis regulator
for 15LO. We discovered that PEBP1, a scaffold
protein inhibitor of protein kinase cascades,
complexes with two 15LO isoforms, 15LO1 and
15LO2, and changes their substrate competence
to generate hydroperoxy-PE. Inadequate reduction
of hydroperoxy-PE due to insufficiency or dysfunction
of a selenoperoxidase, GPX4, leads to
ferroptosis. We demonstrated the importance of
PEBP1-dependent regulatory mechanisms of ferroptotic
death in airway epithelial cells in asthma,
kidney epithelial cells in renal failure, and cortical
and hippocampal neurons in brain trauma. As master
regulators of ferroptotic cell death with profound
implications for human disease, PEBP1/15LO complexes
represent a new target for drug discovery.

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Last Updated On Friday, October 20, 2017 by Orbell, Adam W
Created On Monday, October 02, 2017

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