Exogenous allergic alveolitis: causes and pathogenesis
Last reviewed: 23.04.2024
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Causes of exogenous allergic alveolitis
The development of exogenous allergic alveolitis is caused by the following etiological factors.
- Thermophilic and other bacteria and products of their vital activity (proteins, glycoproteins and lipoproteins, polysaccharides, enzymes, endotoxins).
- Different types of fungi.
- Protein antigens of animal origin (whey proteins and feces of poultry, cattle, pigs, dust containing animal wool particles, an extract of the posterior lobe of the pituitary gland of cattle - adiurecrin, dust of fish meal, products of mites, etc.);
- Antigens of vegetable origin (sawdust of oak, cedar, maple bark, mahogany, moldy straw, cotton and other types of plant dust, extracts of coffee beans, etc.);
- Medicinal products (antibacterial, antiparasitic, anti-inflammatory, enzymatic, radiocontrast and other drugs).
These etiological factors (one or several) are found in certain industries and therefore the various etiological forms of exogenous allergic alveolitis are characteristic for certain professions.
Among the numerous etiologic forms of exogenous allergic alveolitis, the most common are "lung of farmers", "lung of poultry" ("lung of bird lovers"), medicinal allergic alveolitis
Pathogenesis of exogenous allergic alveolitis
In exogenous allergic alveolitis, the particles of organic and inorganic dust penetrating the distal airways and alveoli penetrate antigenic properties and have a size of less than 2-3 microns. In response to this, immunological reactions develop with the participation of both humoral and cellular immunity. The main pathogenetic factors of exogenous allergic alveolitis in general are similar to the pathogenesis of idiopathic fibrosing alveolitis. An allergic reaction develops with the formation of specific antibodies and immune complexes that activate the complement system and alveolar macrophages. The accumulation and peculiar expansion of neutrophilic leukocytes, eosinophils, mast cells, lymphocytes with the release of a number of biologically active substances, which exert a pro-inflammatory and damaging effect on the alveoli, develops under the influence of alveolar macrophage IL-2 and chemotactic factors. Sensitized T-lymphocytes-helpers produce IL-2, under the influence of which are formed from resting T-cell progenitors and cytotoxic T-lymphocytes are activated, inflammatory cell-mediated eaktsiya (delayed-type hypersensitivity reaction). In the development of the inflammatory reaction, an important role is played by the isolation of proteolytic enzymes and active oxygen radicals by alveolar macrophages and neutrophilic leukocytes against the background of a decrease in the activity of the antiproteolytic system. In parallel with the alveolitis, there are processes of granuloma formation, fibroblast activation and fibrosis of the lung interstitium. A huge role in this process is played by alveolar macrophages, producing a factor that induces the growth of fibroblasts and the production of collagen by them.
It should be emphasized that for exogenous allergic alveolitis, atopic IgE-dependent mechanisms (Type I allergic reaction) are not characteristic.
Pathomorphology of exogenous allergic alveolitis
There are acute, subacute and chronic stages (forms) of exogenous allergic alveolitis. The acute stage is characterized by dystrophy and sloughing, desquamation of type I alveolocytes, destruction of the basal membrane, expressed exudation into the cavity of the alveoli, infiltration of the alveoli and interalveolar septa by lymphocytes, plasma cells, histiocytes, edema of the interstitial lung tissue. The damage to the endothelium of the capillaries and their high permeability are also characteristic.
The subacute stage is characterized by less vascular damage, less vivid exudation and the formation of epithelioid-cell noncaseating granulomas in the interstitial lung tissue. Granulomas consist of macrophages, epithelioid, lymphoid, plasma cells. Unlike sarcoidosis, these granulomas are smaller, have no clear boundaries, do not undergo hyalinosis and are localized mainly in interstitium or intra-alveolar. Sarcoidosis is characterized by peribronchial or perivascular localization of granulomas. The subacute form is also characterized by the accumulation of lymphocytes, activated macrophages, and fibroblasts in the interstitial tissue of the lungs.
For the chronic form of exogenous allergic alveolitis, the most significant and significant sign is the proliferation of connective tissue in the interstitial lungs (fibrosing alveolitis) and cystic changes in lung tissue ("honeycomb lung"). At this stage of the process, the granulomas disappear. Infiltration of interstitial lymphocytes, neutrophilic leukocytes is preserved. The morphological picture of exogenous allergic alveolitis in the chronic stage is indistinguishable from idiopathic fibrosing alveolitis.
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