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What causes exogenous allergic alveolitis?
Last reviewed: 06.07.2025
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Causes of exogenous allergic alveolitis
Exogenous allergic alveolitis is caused by inhalation of organic dust containing various antigens, microorganisms (for example, thermophilic actinomycetes from rotted hay, the so-called farmer's lung), aspergilli and penicillium, animal and fish proteins, insect antigens, aerosols of antibiotics, enzymes and other substances. In children, the most common cause of exogenous allergic alveolitis is contact with bird feathers and droppings (the so-called budgerigar lovers' lung or blue-lovers' lung) and elevator dust. In adults, the spectrum of allergens is much wider. for example, cotton dust (babesiosis) or sugar cane dust (bagassosis), sawdust, fungal spores (mushroom growers' lung), fungal dust during cheese production (cheese makers' lung), in patients with diabetes insipidus - inhalation preparations of the posterior pituitary gland, etc. Repeated inhalation of allergens in 5% of those in contact causes the formation of specific antibodies (precipitins) of the IgG class and immune complexes that damage the interstitium of the lung with the development of fibrosis. It is important to emphasize that the presence of atopy in the anamnesis is not a predisposing factor, since the type of allergic reaction in exogenous allergic alveolitis is immune complex.
Pathogenesis of exogenous allergic alveolitis. Unlike atopic bronchial asthma, in which allergic inflammation of the bronchial mucosa is a consequence of the IgE-dependent reaction of type I, the development of exogenous allergic alveolitis is formed with the participation of precipitating antibodies related to immunoglobulins of the IgG and IgM classes. These antibodies, reacting with the antigen, form large-molecular immune complexes that are deposited under the endothelium of the alveolar capillaries. The complement system is activated, fixing on the complexes. In this case, the C1 and C4 fractions of the complement act as mediators of inflammation.
Morphologically, in the acute phase of the disease, changes characteristic of vasculitis are revealed.
With repeated and prolonged exposure to the allergen, sensitized lymphocytes synthesize lymphokines, which are powerful mediators of allergic inflammation. Morphologically, granulomas are determined in this phase, which are transformed into fibrous connective tissue structures, interstitial and alveolar fibrosis is formed, i.e. the disease becomes chronic.