Abstract
Aspergilli are saprophytic fungi widely distributed in nature, and because of their universal presence, all individuals are exposed to these organisms. Among the various members of this genus, Aspergillus fumigatus is associated with over 80% of all human syndromes caused by aspergilli. Saprophytic presence to extensive invasion with this organism has been reported with various intermediary conditions depending on susceptibility and immunocompetence of the host. 55 Other species that have been associated with aspergillosis include A. flavus, A. nidulans, A. niger, A. terreus, A. oryzae, and A. ochraceus. 55,57,72,88 The predominance of A. fumigatus over other aspergilli in human diseases may be due to its ability to grow at human body temperature, its small spore size, and its comparative resistance to oxidative killing. 7,8 Three main processes are involved in the interaction between aspergilli and the lung: colonization, hypersensitivity, and invasion. Colonization is usually a passive process but may lead to immunologic tolerance and local production of potentially toxic fungal metabolites. Allergy or hypersensitivity to Aspergillus antigens depends on the mode and frequency of exposures to the organism as well as on the host immune responses. Aspergillomas (fungus ball) develop in pulmonary cavities secondary to other lung diseases, such as histoplasmosis, tuberculosis, and so forth, whereas invasive aspergillosis is usually associated with underlying defects in host–defense mechanism. 7,8 In this article, we review the recent advances in the field of molecular biology and immunology of Aspergillus allergens and how this new information will lead to enhance the knowledge for better diagnosis and management of allergic aspergillosis.
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