From the Guidelines
Asthma symptoms result from a complex inflammatory process in the airways, involving the release of inflammatory mediators, bronchoconstriction, airway edema, and excessive mucus production, leading to characteristic symptoms of wheezing, coughing, chest tightness, and shortness of breath. The pathophysiology of asthma symptoms is multifaceted, involving various cell types, including mast cells, eosinophils, neutrophils, T lymphocytes, macrophages, and epithelial cells 1. When triggered by allergens, irritants, or other stimuli, these immune cells release inflammatory mediators like histamine, leukotrienes, and cytokines, causing three key changes:
- Bronchial smooth muscle constriction (bronchoconstriction)
- Airway edema
- Excessive mucus production Together, these changes narrow the airways, creating the characteristic symptoms of asthma. The airways also develop hyperresponsiveness, becoming overly sensitive to triggers. In chronic asthma, ongoing inflammation leads to airway remodeling—structural changes including thickening of the airway walls and increased smooth muscle mass—which can cause persistent airflow limitation 1. This pathophysiology explains why asthma treatment focuses on both bronchodilators (like albuterol) to relax airway muscles and anti-inflammatory medications (like inhaled corticosteroids) to reduce the underlying inflammation. Understanding this dual nature of asthma—both inflammatory and bronchoconstrictive—is essential for effective management of the condition. The most recent and highest quality study, published in 2024, highlights the importance of integrating asthma care guidelines into primary care electronic medical records to improve patient outcomes 1.
From the Research
Pathophysiology of Asthma Symptoms
The pathophysiology of asthma symptoms is complex and involves multiple factors, including:
- Inflammation of the pulmonary airways and bronchial hyperresponsiveness, resulting in lower airway obstruction that is usually reversible 2
- Bronchial hyperresponsiveness, documented by decreased bronchial airflow after bronchoprovocation with methacholine or histamine 2
- Triggers that provoke airway obstruction, including cold air, exercise, viral upper respiratory infection, cigarette smoke, and respiratory allergens 2
Inflammatory Process
The inflammatory process in asthma involves:
- Recruitment of leukocytes from the bloodstream to the airway by activated CD4 T-lymphocytes 2
- Release of inflammatory mediators from eosinophils, mast cells, and lymphocytes 2
- Production of interleukin (IL)-4, IL-5, and IL-13 by subclass 2 helper T-lymphocytes 2
- Cross-linkage of two IgE molecules by allergen, causing mast cells to degranulate and release histamine, leukotrienes, and other mediators 2
Airway Remodeling
Airway remodeling, characterized by thickening of all compartments of the airway wall, may have profound consequences on the mechanics of airway narrowing in asthma and contribute to the chronicity and progression of the disease 3
- Repeated cycles of inflammation in the lungs with injury to the pulmonary tissues followed by repair may produce long-term structural changes ("remodeling") of the airways 2
Cellular Infiltrate
The cellular infiltrate in asthma includes:
- Eosinophils, neutrophils, lymphocytes, and plasma cells in the bronchial tissues, bronchial secretions, and mucus 2
- Lymphocytes and eosinophils constitute most of the inflammatory cells infiltrating the bronchial mucosa 4
- Mast cells, macrophages, and neutrophils also play a role in the inflammatory process 5, 4
Cytokines and Mediators
Cytokines and mediators involved in the pathogenesis of asthma include: