Impacts and Immune Mechanisms of Pollutant-Mediated Asthma and Airway Inflammation.
- 1Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea.
- 2Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea. [email protected].
Abstract
Air pollution is a major environmental risk factor contributing to the development, exacerbation, and persistence of asthma. A wide range of airborne pollutants, including particulate matter (PM), ozone (O₃), nitrogen dioxide, sulfur dioxide, diesel exhaust particles (DEPs), volatile organic compounds, and biological contaminants, can interact with the airway epithelium and immune system, leading to dysregulated inflammatory responses. Increasing evidence indicates that pollutant exposure induces epithelial injury, disrupts epithelial barrier integrity, promotes oxidative stress, and activates innate immune signaling pathways. These upstream events shape downstream adaptive immune responses and contribute to heterogeneous inflammatory patterns in asthma, including type 2 eosinophilic inflammation, non-type 2 neutrophilic inflammation, and mixed inflammatory phenotypes associated with severe or corticosteroid-resistant asthma. At the cellular and molecular levels, pollutants activate pattern-recognition receptors and redox-sensitive signaling cascades, including nuclear factor-kappa B, mitogen-activated protein kinase, PI3K/Akt, and inflammasome pathways. These cascades promote epithelial alarmin release, proinflammatory cytokine production, T-cell polarization, neutrophil recruitment, airway hyperresponsiveness, mucus hypersecretion, and structural remodeling. Pollutant-specific mechanisms, such as PM-induced NOD-like receptor family pyrin domain-containing protein 3 inflammasome activation, O₃-mediated epithelial barrier disruption, DEP-driven interleukin-17A responses, and pollutant-allergen co-exposure, further contribute to the heterogeneity of pollutant-mediated asthma. While experimental models have provided valuable mechanistic insights, differences in exposure dose, duration, pollutant composition, and host immune context limit direct translation to real-world human exposure scenarios. This review summarizes current evidence on the impacts of air pollutants on asthma and the immune mechanisms underlying pollutant-mediated asthma. A better understanding of these epithelial-immune pathways may support improved risk assessment, prevention, and more personalized management of asthma in the context of increasing environmental pollution.
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BibTeX
@article{yoon2026impacts,
title = {{Impacts and Immune Mechanisms of Pollutant-Mediated Asthma and Airway Inflammation.}},
author = {Sang-Min Yoon and Min-Hyeok An and Pureun-Haneul Lee and An-Soo Jang},
journal = {Allergy, asthma \& immunology research},
year = {2026},
month = sep,
doi = {10.4168/aair.2026.18.5.640},
url = {https://europepmc.org/article/MED/42845222},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Impacts and Immune Mechanisms of Pollutant-Mediated Asthma and Airway Inflammation.
AU - Sang-Min Yoon
AU - Min-Hyeok An
AU - Pureun-Haneul Lee
AU - An-Soo Jang
PY - 2026
DA - 2026/09/01
JO - Allergy, asthma & immunology research
DO - 10.4168/aair.2026.18.5.640
UR - https://europepmc.org/article/MED/42845222
AB - Air pollution is a major environmental risk factor contributing to the development, exacerbation, and persistence of asthma. A wide range of airborne pollutants, including particulate matter (PM), ozone (O₃), nitrogen dioxide, sulfur dioxide, diesel exhaust particles (DEPs), volatile organic compounds, and biological contaminants, can interact with the airway epithelium and immune system, leading to dysregulated inflammatory responses. Increasing evidence indicates that pollutant exposure induces epithelial injury, disrupts epithelial barrier integrity, promotes oxidative stress, and activates innate immune signaling pathways. These upstream events shape downstream adaptive immune responses and contribute to heterogeneous inflammatory patterns in asthma, including type 2 eosinophilic inflammation, non-type 2 neutrophilic inflammation, and mixed inflammatory phenotypes associated with severe or corticosteroid-resistant asthma. At the cellular and molecular levels, pollutants activate pattern-recognition receptors and redox-sensitive signaling cascades, including nuclear factor-kappa B, mitogen-activated protein kinase, PI3K/Akt, and inflammasome pathways. These cascades promote epithelial alarmin release, proinflammatory cytokine production, T-cell polarization, neutrophil recruitment, airway hyperresponsiveness, mucus hypersecretion, and structural remodeling. Pollutant-specific mechanisms, such as PM-induced NOD-like receptor family pyrin domain-containing protein 3 inflammasome activation, O₃-mediated epithelial barrier disruption, DEP-driven interleukin-17A responses, and pollutant-allergen co-exposure, further contribute to the heterogeneity of pollutant-mediated asthma. While experimental models have provided valuable mechanistic insights, differences in exposure dose, duration, pollutant composition, and host immune context limit direct translation to real-world human exposure scenarios. This review summarizes current evidence on the impacts of air pollutants on asthma and the immune mechanisms underlying pollutant-mediated asthma. A better understanding of these epithelial-immune pathways may support improved risk assessment, prevention, and more personalized management of asthma in the context of increasing environmental pollution.
SN - 2092-7355
SN - 2092-7363
ER -