Related Experiment Video
Updated: Dec 13, 2025
Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
Published on: September 20, 2024
Continuous exposure of PM2.5 exacerbates ovalbumin-induced asthma in mouse lung via a JAK-STAT6 signaling pathway
Yonghui Yang1, Xiaoxia Li1, Xiaoying An2
1Department of Pathology, Hebei Province Chest Hospital, Lung Cancer Prevention and Control Center of Hebei Province, Shijiazhuang, China.
Background:
Epidemiological studies and mice models have demonstrated that air pollution containing particulate matter smaller than 2.5 μm (PM2.5) exacerbates acute episodes of asthma in both children and adults.
Objectives:
To investigate the effect of continuous PM2.5 treatment on asthma regulation mechanism behind this effect.
Material And Methods:
In this study, the effects of continuous exposure to PM2.5 on asthma and eosinophil recruitment was compared to the effect of a single pre-ovalbumin (OVA)-sensitization exposure to PM2.5. Wild-type mice were either challenged once with PM2.5 + OVA before sensitization and asthma induction over a 27-day period, or with 5 times of PM2.5 + OVA treatment and sensitization/asthma induction over the same period.
Results:
Continuous exposure to PM2.5 significantly increased total plasma immunoglobulin E (IgE), bronchial alveolar lavage fluid (BALF) cell numbers, eosinophils, and macrophages, leading to increased lung injury. This effect was regulated through increased production of chemokines and cytokines, such as interleukin (IL)-1β, monocyte chemoattractant protein 1 (MCP-1), IL-12, IL-5, IL-13, and prostaglandin D2 (PGD2). Eosinophil recruitment during continuous PM2.5 treatment was regulated through phosphorylation of the JAK/STAT6 pathway. As this study shows, continuous PM2.5 treatment significantly worsens asthma as compared to single exposure to PM2.5 or OVA exposure alone.
Conclusions:
Our findings reveal that continuous exposure of PM2.5 exacerbates OVA-induced asthma in mouse lung through JAK-STAT6 signaling pathway.
Insights
Continuous exposure to fine particulate matter (PM2.5) significantly worsens asthma by increasing lung inflammation and injury. This exacerbation is mediated by the JAK-STAT6 signaling pathway, highlighting the detrimental effects of prolonged air pollution exposure.
Area of Science:
- Environmental Health
- Immunology
- Respiratory Medicine
Background:
- Air pollution, specifically fine particulate matter (PM2.5), is known to worsen asthma in humans.
- Epidemiological studies and animal models link PM2.5 exposure to acute asthma exacerbations.
Purpose of the Study:
- To investigate how continuous PM2.5 exposure affects asthma regulation.
- To compare the impact of continuous PM2.5 exposure versus single exposure on asthma mechanisms.
Main Methods:
- Wild-type mice were subjected to either single or five exposures of PM2.5 and ovalbumin (OVA) over 27 days.
- Asthma induction and eosinophil recruitment were assessed under continuous and single PM2.5 exposure conditions.
Main Results:
- Continuous PM2.5 exposure significantly elevated total IgE, inflammatory cells (eosinophils, macrophages) in BALF, and lung injury.
- Increased production of cytokines (IL-1β, MCP-1, IL-12, IL-5, IL-13) and PGD2 was observed.
- Eosinophil recruitment was regulated via the JAK/STAT6 pathway phosphorylation.
Conclusions:
- Continuous PM2.5 exposure exacerbates OVA-induced asthma in mice.
- The JAK-STAT6 signaling pathway plays a crucial role in mediating PM2.5-induced asthma exacerbation.
Related Concept Videos
01:26Asthma-II: Pathophysiology and Classification
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
01:20Asthma: Pathogenesis and Management
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
01:29Asthma-I: Introduction
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
01:25Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
01:24Asthma-III: Symptoms and Complications
Classification of Asthma