What Is Alveolitis?

In medicine, farmers' lungs should be called "exogenous allergic alveolitis" or "allergic alveolitis". The causes of exogenous allergic alveolitis are many common organic dusts including actinomycetes and fungal spores, animal and plant proteins, bacteria and their products, insect antigens, and certain chemicals. The antigenic properties of some dusts have not yet been determined. It is generally believed that the cause of farmers' lungs is mainly ordinary high temperature actinomycetes. In recent years, domestic scholars have successively reported another strain of thermophilic actinomycetes related to farmers' lungs, heat-absorbing water streptomyces. Among many antigens, thermophilic actinomycetes are the most common and important, especially micropolyspores followed by ordinary High temperature actinomycetes. The fungus has the form of a fungus, but it belongs to bacteria that produce a large amount of compost, soil, food, and contaminated water in moist, warm, and moldy organic matter. The bacteria are often prone to disease by inhaling moldy hay, cereals, and bagasse. There are many thermophilic actinomycetes in the fertilizers for mushroom cultivation and in the air of the production environment, and ordinary high temperature actinomycetes are the main ones. Inhalers of the growers can cause mushrooms to work. Poultry breeder's lungs (such as pigeon feeders, parrot workers, etc.) are caused by bird serum, bird droppings, bird feather powder, and bird eggs. Some people think that the powder on pigeon feathers is about 1 m in size. Keratin particle antigen, its pathogenic effect is more important than pigeon serum and excreta. In addition, domestic reports of silk textile workers inhaling mulberry silk dust (possibly sericin) in the air of the workshop may cause allergic alveolar humidifiers and air conditioners. The cause of the lungs is white thermophilic actinomycetes. After inhalation of toluene diisocyanate phthalic anhydride, which is widely used in the chemical industry, its hapten effect may also cause allergic alveolitis. Regarding tobacco growers 'tea growers' disease, etc., its antigenic properties have not been fully understood.

Exogenous allergic alveolitis

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In medicine, farmers' lungs should be called "exogenous allergic alveolitis" or "allergic alveolitis". The causes of exogenous allergic alveolitis are many common organic dusts including actinomycetes and fungal spores, animal and plant proteins, bacteria and their products, insect antigens, and certain chemicals. The antigenic properties of some dusts have not yet been determined. It is generally believed that the cause of farmers' lungs is mainly ordinary high temperature actinomycetes. In recent years, domestic scholars have successively reported another strain of thermophilic actinomycetes related to farmers' lungs, heat-absorbing water streptomyces. Among many antigens, thermophilic actinomycetes are the most common and important, especially micropolyspores followed by ordinary High temperature actinomycetes. The fungus has the form of a fungus, but it belongs to bacteria that produce a large amount of compost, soil, food, and contaminated water in moist, warm, and moldy organic matter. The bacteria are often prone to disease by inhaling moldy hay, cereals, and bagasse. There are many thermophilic actinomycetes in the fertilizers for mushroom cultivation and in the air of the production environment, and ordinary high temperature actinomycetes are the main ones. Inhalers of the growers can cause mushrooms to work. Poultry breeder's lungs (such as pigeon feeders, parrot workers, etc.) are caused by bird serum, bird droppings, bird feather powder, and bird eggs. Some people think that the powder on pigeon feathers is about 1 m in size. Keratin particle antigen, its pathogenic effect is more important than pigeon serum and excreta. In addition, domestic reports of silk textile workers inhaling mulberry silk dust (possibly sericin) in the air of the workshop may cause allergic alveolar humidifiers and air conditioners. The cause of the lungs is white thermophilic actinomycetes. After inhalation of toluene diisocyanate phthalic anhydride, which is widely used in the chemical industry, its hapten effect may also cause allergic alveolitis. Regarding tobacco growers 'tea growers' disease, etc., its antigenic properties have not been fully understood.

Chinese name

Exogenous allergic alveolitis

Subject

medicine

Cause

Animal and plant protein

Alias

Exogenous allergic alveolitis

Important mechanism

In recent years, exogenous allergic alveolitis is considered to be an important mechanism of immune complex disease type III allergy, and also involves type IV allergy. The activation of the complement system has important significance and activated alveolar macrophages may be the central link of the pathogenesis.

(1) The complement-mediated type allergic reaction occurs in the sensitized individual 4-8 hours after re-exposure to the antigen, and Arthus reaction can occur 4-6 hours after intradermal injection of the antigen. Precipitation of complement. In most patients, the corresponding antigen can be found in the precipitation of antibodies (genus IgG). The use of antigens as a bronchial challenge test can show the same changes in lung function as clinical exogenous allergic alveolitis. Therefore, this disease is related to complement-mediated type allergies, and immune complexes are of great significance.

(B) T lymphocyte-mediated type IV allergy In recent years, it has been noted that type IV allergy plays an important role in the pathogenesis of this disease. Patients with pulmonary histopathology have caseous granulomatous formation, and lymphocytes can meet the corresponding antigenic capacity in vitro. Produces macrophage migration inhibitory factor (MIF). Animal experiments found that sensitized T lymphocytes were implanted in experimental animals, and then inhaled by antigen to stimulate, causing lung damage similar to human exogenous allergic alveolitis. Bronchial alveolar lavage in patients with exogenous allergic alveolitis An increase in lymphokine was also found in the fluid. The above findings support the role of type allergy in the pathogenesis of this disease.

(3) The role of local macrophages The use of moldy B. subtilis and micropolysporum can directly stimulate alveolar macrophages and cause proteolytic enzymes to release and lyse C3 and release C3b. The latter binds to complement receptors on the surface of macrophages, which further activates macrophages to produce lung tissue lesions including granuloma formation.

At present, it is tended to think that exogenous allergic alveolitis is mainly changed from type III allergy and then to type IV allergy, and macrophage activation and the resulting inflammatory response can be caused by non-immune pathways. Lung injury but many details are unclear