Immunologic mechanism of allergic diseases in airway is known to be concerned with allergic response of Type I, III or IV and mainly allergic response of Type I by IgE antibody (or occasionally IgG4 antibody).
On this occasion, various chemical mediators released from mast cells by antigen-antibody reaction affect the upper and lower airways, and induce inflammatory change.
The function of the cells such as macrophage, lymphocyte, basophils, eosinophils and monocytes which take part of the allegic inflammation have been confirmed. Histamin, SRS-A, ECF-A, prostaglandins (PG), PAF, NCF and leucotrienes (LT) are also thought as chemical mediators. PGF2α, LTC4 and LTD4 are concerned as a factor of hyperresponse in airway.
Recent studies suggest that major basic protein (MBP) in granule of eosinophilis induce the inflammation on bronchial epitherium, accelerate the release of LT from the mast cell and increase the bronchial spasms and secretion of bronchial gland.
Eosinophilis and neutrophilis which act as inflammatory cells are thought to cause late phase asthmatic response.
Concerning the treatment, drugs to have the supressive function of the chemical mediators by means of cell membrane of mast cell, LT and anti-LT agents based on the immunopathologic mechanism discussed above have been developed.
