Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
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:
In summary, asthma results from an exaggerated immune response in the airways, leading to inflammation, bronchoconstriction, and remodeling. These contribute to typical symptoms like wheezing, coughing, and shortness of breath. Asthma management involves medications targeting these mechanisms, and avoiding triggers.
Asthma involves airway inflammation and increased sensitivity, often caused by allergens and irritants.
When an individual is exposed to allergens, the body activates immune cells—including mast cells, macrophages, eosinophils, neutrophils, T and B lymphocytes, and airway epithelial cells—leading to chronic inflammation.
This triggers the production of allergen-specific IgE antibodies that attach to mast cells. Upon repeated exposure, allergens bind to IgE on mast cells, releasing inflammatory mediators such as histamine , cytokines, leukotrienes, and prostaglandins.
These mediators recruit eosinophils, lymphocytes, and neutrophils, causing bronchoconstriction, vascular congestion, edema, and mucus secretion, all contributing to airway obstruction.
Asthma involves nerve-related changes in the airways, which, when triggered by allergens or irritants, lead to increased muscle contraction, mucus secretion, and airway narrowing.
Persistent inflammation can cause airway remodeling, including fibrosis, muscle hypertrophy, mucus hypersecretion, inflammation, and angiogenesis.
繁體中文
