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Causes of bronchial asthma in children
Last reviewed: 04.07.2025
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Three groups of factors are important in the development of bronchial asthma:
- genetically determined predisposition of the child's body to allergic reactions;
- sensitization by exo- and endoallergens;
- environmental factors that alter the body's immunobiological reactivity.
A study of families of children with bronchial asthma shows that the total contribution of genetic factors to the development of bronchial asthma is 82%.
A cluster of genes that play a role in the development of bronchial asthma, encoding Th 2 -cytokines, is located on the long arm of chromosome 5 (5q31.1-5q33). This same region includes the beta-adrenergic receptor gene, which is responsible for changes in bronchial reactivity in asthma.
The dominant atopy gene encoding the B-chain of the high-affinity receptor to IgE is located on the long arm of chromosome 11 in the llql3 region. The gene whose product is a protein - phospholipase-A inhibitor, involved in the synthesis of prostaglandins and leukotrienes - the main mediators of inflammation in bronchial asthma, is mapped in the same region.
Genetic control of the specific IgE response to allergen exposure is carried out by a group of genes localized in the 6q21.3 region.
An atopy-independent inheritance of bronchial hyperreactivity has been established. A hereditary defect in the synthesis of beta-adrenoreceptors is confirmed by a greater sensitivity of patients with bronchial asthma to adrenomimetics than patients with acute viral obstructive bronchitis.
Congenital predisposition forms internal causes of the disease - biological defects that can be genetically determined and also formed during pregnancy.
Sensitization of the respiratory tract is caused by inhalation allergens - household, epidermal, fungal, pollen. Among household allergens - dust, hair of domestic animals (dogs, cats), flowers, down, feather pillows, blankets, etc. Among pollen allergens - trees, shrubs, cereals.
Medicines: antibiotics, especially penicillin, vitamins, serums, acetylsalicylic acid (less common in children).
The pathogenesis of bronchial asthma is primarily based on immunological reactions involving mast cells and basophils, eosinophils, and T-lymphocytes.
Under the influence of allergenic stimuli, activation of a subpopulation of T-lymphocytes occurs with subsequent release of interleukins (4,6,10,13), inducing hyperproduction of specific IgE, leading to the release of histamine, eosinophil chemotactic factor; stimulation of leukotrienes, prostaglandins (PGE2), platelet activating factor, thromboxane.
Leukotrienes are part of a slow-acting substance that causes prolonged contraction of bronchial smooth muscles, increases mucus secretion, and reduces contraction of the cilia of the ciliated epithelium. Platelet activating factor causes platelet aggregation, microcirculation disorders, and migration of neutrophils and eosinophils.
A decrease in total and secretory IgA is of great importance in pathogenesis.
An imbalance in the functional state of the sympathetic and parasympathetic divisions of the higher nervous system plays a major role in pathogenesis.
As the severity of bronchial asthma increases, the number of causative factors that provoke an attack of bronchial asthma increases. One of these factors that plays a role in the pathogenesis of bronchial asthma is ARVI. Affecting the mucous membrane of the bronchi, it disrupts the barrier function, facilitating the penetration of exoallergens, and also leads to the development of bronchial hyperreactivity.
In such cases, we should talk about infectious dependence as one of the variants of trigger factors. The so-called triggers that cause exacerbations of bronchial asthma, stimulate inflammation in the bronchi and provoke the development of acute bronchospasm are allergens, viral infections, cold air, tobacco smoke, emotional stress, physical exertion, meteorological factors.
[ Pathomorphology of bronchial asthma
During an attack of bronchial asthma, there is a spasm of the smooth muscles of the lungs and large bronchi, swelling of the bronchial walls, accumulation of mucus in the lumen of the respiratory tract, cellular infiltration of the submucous membrane and thickening of the basement membrane.