Which immunologic mechanism is usually involved in bronchial asthma?

In bronchial asthma, the primary immunologic mechanism involved is immediate hypersensitivity, also known as type I hypersensitivity. This response is primarily mediated by immunoglobulin E (IgE) antibodies. When an individual with asthma is exposed to certain allergens, such as pollen, dust mites, or pet dander, these allergens provoke the activation of IgE. This activation leads to the degranulation of mast cells and basophils, releasing various mediators like histamines, leukotrienes, and prostaglandins. These mediators cause bronchoconstriction, increased mucus production, and inflammation, resulting in the classic symptoms of asthma such as wheezing, shortness of breath, chest tightness, and coughing.

This mechanism is distinguishable from other hypersensitivity reactions. For instance, delayed hypersensitivity, characterized by a slower immune response involving T cells, is typically associated with conditions like contact dermatitis. Type III hypersensitivity involves immune complex formation and is more relevant in conditions like systemic lupus erythematosus. Type II hypersensitivity involves antibody-mediated destruction of target cells and is typically seen in autoimmune diseases or certain transfusion reactions. Therefore, the characterization of bronchial asthma as an immediate hypersensitivity reaction highlights the rapid and acute nature