Nociceptor Neurons Control Pollution-Mediated Neutrophilic Asthma DOI Open Access

Jo-Chiao Wang,

Théo Crosson,

Amin Reza Nikpoor

et al.

Published: Oct. 21, 2024

The immune and sensory nervous systems, having evolved together, use a shared language of receptors transmitters to maintain homeostasis by responding external internal disruptions. Although beneficial in many cases, neurons can exacerbate inflammation during allergic reactions, such as asthma. Our research modeled asthma aggravated pollution, exposing mice ambient PM 2.5 particles ovalbumin. This exposure significantly increased bronchoalveolar lavage fluid neutrophils γδ T cells compared ovalbumin alone. We normalized airway lung neutrophil levels silencing nociceptor at inflammation’s peak using intranasal QX-314 or ablating TRPV1-expressing neurons. Additionally, we observed heightened sensitivity chemical-sensing TRPA1 channels from pollution-exacerbated asthmatic mice. Elevated artemin were detected the pollution-exposed mice, with normalizing ablated Upon particles, alveolar macrophages expressing pollution-sensing aryl hydrocarbon receptors, identified source artemin. molecule enhanced responsiveness influx, providing novel mechanism which lung-innervating respond air pollution suggesting potential therapeutic target for controlling neutrophilic asthma, clinically intractable condition.

Language: Английский

Wildfire Risk Mitigation through Systems Analysis of the Planetary Emergency DOI Creative Commons
James H. Lambert,

R. Dorn,

Bilal M. Ayyub

et al.

ASCE OPEN Multidisciplinary Journal of Civil Engineering, Journal Year: 2024, Volume and Issue: 2(1)

Published: Dec. 19, 2024

Language: Английский

Citations

1
Evaluating Chemical Transport and Machine Learning Models for Wildfire Smoke PM2.5: Implications for Assessment of Health Impacts DOI
Minghao Qiu, Makoto Kelp, Sam Heft-Neal

et al.

Environmental Science & Technology, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 18, 2024

Growing wildfire smoke represents a substantial threat to air quality and human health. However, the impact of on health remains imprecisely understood due uncertainties in both measurement exposure population dose-response functions linking Here, we compare daily smoke-related surface fine particulate matter (PM

Language: Английский

Citations

1
Nociceptor Neurons Control Pollution-Mediated Neutrophilic Asthma DOI Creative Commons

Jo-Chiao Wang,

Théo Crosson,

Amin Reza Nikpoor

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 23, 2024

ABSTRACT The immune and sensory nervous systems, having evolved together, use a shared language of receptors transmitters to maintain homeostasis by responding external internal disruptions. Although beneficial in many cases, neurons can exacerbate inflammation during allergic reactions, such as asthma. Our research modeled asthma aggravated pollution, exposing mice ambient PM 2.5 particles ovalbumin. This exposure significantly increased bronchoalveolar lavage fluid neutrophils γδ T cells compared ovalbumin alone. We normalized airway lung neutrophil levels silencing nociceptor at inflammation’s peak using intranasal QX-314 or ablating TRPV1-expressing neurons. Additionally, we observed heightened sensitivity chemical-sensing TRPA1 channels from pollution-exacerbated asthmatic mice. Elevated artemin were detected the pollution-exposed mice, with normalizing ablated Upon particles, alveolar macrophages expressing pollution-sensing aryl hydrocarbon receptors, identified source artemin. molecule enhanced responsiveness influx, providing novel mechanism which lung-innervating respond air pollution suggesting potential therapeutic target for controlling neutrophilic asthma, clinically intractable condition.

Language: Английский

Citations

0
Nociceptor Neurons Control Pollution-Mediated Neutrophilic Asthma DOI Open Access

Jo-Chiao Wang,

Théo Crosson,

Amin Reza Nikpoor

et al.

Published: Oct. 21, 2024

The immune and sensory nervous systems, having evolved together, use a shared language of receptors transmitters to maintain homeostasis by responding external internal disruptions. Although beneficial in many cases, neurons can exacerbate inflammation during allergic reactions, such as asthma. Our research modeled asthma aggravated pollution, exposing mice ambient PM 2.5 particles ovalbumin. This exposure significantly increased bronchoalveolar lavage fluid neutrophils γδ T cells compared ovalbumin alone. We normalized airway lung neutrophil levels silencing nociceptor at inflammation’s peak using intranasal QX-314 or ablating TRPV1-expressing neurons. Additionally, we observed heightened sensitivity chemical-sensing TRPA1 channels from pollution-exacerbated asthmatic mice. Elevated artemin were detected the pollution-exposed mice, with normalizing ablated Upon particles, alveolar macrophages expressing pollution-sensing aryl hydrocarbon receptors, identified source artemin. molecule enhanced responsiveness influx, providing novel mechanism which lung-innervating respond air pollution suggesting potential therapeutic target for controlling neutrophilic asthma, clinically intractable condition.

Language: Английский

Citations

0
Nociceptor Neurons Control Pollution-Mediated Neutrophilic Asthma DOI Open Access

Jo-Chiao Wang,

Théo Crosson,

Amin Reza Nikpoor

et al.

Published: Oct. 21, 2024

The immune and sensory nervous systems, having evolved together, use a shared language of receptors transmitters to maintain homeostasis by responding external internal disruptions. Although beneficial in many cases, neurons can exacerbate inflammation during allergic reactions, such as asthma. Our research modeled asthma aggravated pollution, exposing mice ambient PM 2.5 particles ovalbumin. This exposure significantly increased bronchoalveolar lavage fluid neutrophils γδ T cells compared ovalbumin alone. We normalized airway lung neutrophil levels silencing nociceptor at inflammation’s peak using intranasal QX-314 or ablating TRPV1-expressing neurons. Additionally, we observed heightened sensitivity chemical-sensing TRPA1 channels from pollution-exacerbated asthmatic mice. Elevated artemin were detected the pollution-exposed mice, with normalizing ablated Upon particles, alveolar macrophages expressing pollution-sensing aryl hydrocarbon receptors, identified source artemin. molecule enhanced responsiveness influx, providing novel mechanism which lung-innervating respond air pollution suggesting potential therapeutic target for controlling neutrophilic asthma, clinically intractable condition.

Language: Английский

Citations

0