Etiology and risk factors
The development of the disease is driven by a complex interplay between genetic predisposition and environmental factors. In pediatric practice, the allergic (atopic) form predominates, whereas non-allergic or obesity-related asthma is significantly less common.
All factors influencing the development and course of the pathology are divided into groups:
- Intrinsic (endogenous) factors: form the foundational basis. These include genetics, atopy, patient sex, and baseline bronchial hyperresponsiveness.
- Extrinsic (exogenous) factors: act as catalysts for the predisposition. These include various allergens, bacterial and viral infections, tobacco smoke, and socio-economic conditions.
- Exacerbation triggers: direct instigators of attacks (allergen contact, acute respiratory viral infections).
It is important to highlight fetal/prenatal risk factors. It has been reliably proven that maternal smoking during pregnancy leads to an initial decrease in lung function in the newborn, creating a high predisposition to bronchoconstrictive syndrome.
Pathogenesis of chronic inflammation
A key role in the inflammatory cascade is played by the Th2 type of immune response. The process is triggered when dendritic cells capture an allergen and present it to T lymphocytes. This penetration is frequently facilitated by defects in the epithelial barrier function.
Activated Th2 cells release cytokines (specifically IL-4 and IL-13), which stimulate B lymphocytes to massively produce IgE antibodies. This entire complex network of cytokine and transcription factor interactions is under strict genetic control. In addition to Th2 cells, inflammation regulation involves Th1, Th17, regulatory Treg, and Th9 lymphocytes.
The inflammation is predominantly eosinophilic in nature and develops in several stages:
- Effector activation: the allergen binds to IgE fixed on mast cell and basophil receptors (FcεRI and FcεRII). Degranulation occurs with the release of histamine, bradykinin, leukotrienes, and platelet-activating factor.
- Chemotaxis: cytokines and eotaxin attract new immune cells to the focus.
- Infiltration: the bronchial wall becomes infiltrated by T lymphocytes, dendritic cells, and eosinophils. Structural elements such as epithelial cells, fibroblasts, and endothelial cells are also actively involved in the process.
Mechanisms of obstruction and bronchial remodeling
Clinical manifestations (paroxysmal cough, expiratory dyspnea, wheezing, chest tightness) are caused by the narrowing of the airway lumen. This obstruction consists of three components:
- Bronchospasm of the smooth muscle;
- Edema of the mucous membrane;
- Hypersecretion of viscous mucus.
With prolonged chronicity, chronic inflammation and ongoing epithelial cell death lead to remodeling—an irreversible structural alteration of the bronchial wall. Morphologically, this manifests as thickening of the subepithelial reticular basement membrane, neoangiogenesis (formation of new blood vessels), and a protease-antiprotease imbalance.
Role of viruses and bronchial hyperresponsiveness
Respiratory viruses (especially rhinovirus, parainfluenza, and RSV) are major triggers of bronchial obstruction in young children. Viral impact stimulates vagus nerve afferent endings, triggering a neurogenic mechanism of inflammation.
Children with asthma exhibit a deficiency in interferon-γ, which impairs epithelial antiviral defense, causes cytotoxic cell death, and promotes prolonged viral persistence. This explains the protracted course of acute respiratory viral infections in such patients.
A typical feature of pediatric asthma is bronchial hyperresponsiveness (BHR)—spasm in response to nonspecific stimuli such as cold air, physical exertion (body warm-up), or emotional stress. BHR develops due to epithelial barrier disruption, parasympathetic activation, and impaired heat and moisture exchange within the mucosa. As the child grows and achieves medical control, BHR may gradually decrease.
For quick memorization of the three components of bronchial obstruction, use the acronym SEH: Spasm (bronchospasm), Edema (mucosal), Hypersecretion (mucus).
Class and exam questions
Is virus-induced obstruction in infancy a 100% guarantee of developing asthma?
No. Although viruses are a potent primary trigger, not all children with episodes of virus-induced obstruction at an early age develop asthma.
What rare forms of bronchial obstruction can occur under the influence of triggers?
Cholinergic (triggered by internal warm-up/temperature), contact (upon skin contact with a trigger), and extremely rare aquagenic (upon contact with water) forms are distinguished.
Why do acute respiratory viral infections run a more severe and protracted course in children with asthma?
This is associated with local immunodeficiency: in asthma, the ability of the respiratory epithelium to produce interferon-γ is reduced, which facilitates the unimpeded spread (dissemination) of the virus.
What else to study on this topic
- Detailed role of interleukins (IL-4, IL-13) in switching B lymphocytes to IgE synthesis
- Structure and functions of FcεRI (type I) and FcεRII (type II) receptors
- Protease-antiprotease imbalance in bronchial remodeling
- Mechanisms of neurogenic inflammation via stimulation of vagal receptors
- Pathophysiology of contact, aquagenic, and cholinergic forms of asthma
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Other topics in "Chapter 5. Allergic Diseases"
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