In asthma, which type of hypersensitivity reaction is primarily involved?

Asthma is primarily associated with Type I hypersensitivity reactions, which are mediated by Immunoglobulin E (IgE). In this form of hypersensitivity, an individual is exposed to an allergen, leading to the production of IgE antibodies. These IgE antibodies bind to mast cells and basophils, sensitizing them to future exposures to the same allergen. Upon subsequent exposure, the allergen cross-links the IgE on these cells, resulting in their degranulation and the release of various inflammatory mediators, such as histamine, leukotrienes, and prostaglandins. This process leads to the characteristic symptoms of asthma, including broncho-constriction, airway inflammation, and increased mucus production, all of which contribute to the difficulty in breathing experienced by individuals with asthma.

In contrast, Type II hypersensitivity involves cytotoxic antibodies that target specific cells, typically resulting in cell destruction. Type III hypersensitivity involves immune complexes that can deposit in tissues, triggering an inflammatory response. Type IV hypersensitivity, also known as delayed-type hypersensitivity, is mediated by T cells rather than antibodies and involves a delayed response to antigens.

Thus, the nature of the immune response in asthma aligns with the mechanisms associated with Type I hypersensitivity