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DEVELOPMENT MECHANISM AND TREATMENT METHODS OF ALLERGIC
RHINITIS AND BRONCHIAL ASTHMA
Hamidov Bahodir Obidjon o’g’li
Faculty of Medicine, International University of Asia, Uzbekistan.
https://doi.org/10.5281/zenodo.17197682
Abstract. Allergic rhinitis is an IgE-mediated inflammatory response of the nasal mucosa
to allergens such as pollen, dust mites, mold, or animal dander. Bronchial asthma is a chronic
inflammatory disease of the airways characterized by hyperresponsiveness, reversible airflow
obstruction, and recurrent episodes of wheezing, breathlessness, and coughing.
Keywords: APCs, Mast cell activation, Chronic inflammation, Airway hyperreactivity,
β2-agonists.
Introduction
Allergic rhinitis (AR) and bronchial asthma (BA) are chronic inflammatory diseases of
the respiratory system that often coexist and share common immunopathological mechanisms.
Both conditions significantly affect the quality of life, productivity, and overall health of
patients worldwide. Understanding their development mechanisms and modern treatment
strategies is crucial for effective management.
Development Mechanism
Allergic Rhinitis
Allergic rhinitis is an IgE-mediated inflammatory response of the nasal mucosa to
allergens such as pollen, dust mites, mold, or animal dander.
Pathogenesis:
Sensitization phase – Initial exposure to allergens activates antigen-presenting cells
(APCs), leading to T-helper 2 (Th2) cell activation.
IgE production – Th2 cells stimulate B lymphocytes to produce allergen-specific IgE
antibodies.
Mast cell activation – IgE binds to mast cells, and upon re-exposure, allergen cross-links
IgE receptors, leading to mast cell degranulation.
Release of mediators – Histamine, leukotrienes, prostaglandins, and cytokines cause
sneezing, nasal congestion, rhinorrhea, and itching.
Chronic inflammation – Eosinophils and other inflammatory cells infiltrate the mucosa,
leading to persistent symptoms.
Bronchial Asthma
Bronchial asthma is a chronic inflammatory disease of the airways characterized by
hyperresponsiveness, reversible airflow obstruction, and recurrent episodes of wheezing,
breathlessness, and coughing.
Pathogenesis:
Sensitization and IgE response – Similar to AR, allergens induce IgE production and
mast cell activation.
Acute phase reaction – Histamine and leukotrienes cause bronchoconstriction, increased
vascular permeability, and mucus secretion.
Chronic inflammation – Persistent recruitment of eosinophils, Th2 cells, and mast cells
contributes to airway remodeling.
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Airway hyperreactivity – Smooth muscle hypertrophy, goblet cell hyperplasia, and
basement membrane thickening lead to exaggerated bronchial responses to triggers.
Treatment Methods
Allergic Rhinitis
1. Allergen avoidance – Reducing exposure to dust mites, pollen, pets, and irritants.
2. Pharmacotherapy:
Antihistamines (e.g., loratadine, cetirizine) – reduce sneezing and itching.
Intranasal corticosteroids (e.g., fluticasone, mometasone) – most effective for nasal
inflammation.
Decongestants – provide temporary relief of nasal obstruction.
Leukotriene receptor antagonists (e.g., montelukast) – especially useful in patients with
concomitant asthma.
3.Allergen immunotherapy (AIT): Subcutaneous or sublingual administration of allergens
to induce tolerance and modify disease progression.
Bronchial Asthma
1.Trigger control – Avoiding allergens, smoke, pollutants, and occupational irritants.
2. Pharmacotherapy:
Short-acting β2-agonists (SABA) – rescue therapy for acute attacks.
Inhaled corticosteroids (ICS) – cornerstone of long-term control.
Long-acting β2-agonists (LABA) – used with ICS for moderate-to-severe asthma.
Leukotriene receptor antagonists – for mild asthma or add-on therapy.
Biological agents – anti-IgE (omalizumab), anti-IL-5 (mepolizumab), anti-IL-4/13
(dupilumab) for severe refractory asthma.
3. Non-pharmacological approaches:
Pulmonary rehabilitation and breathing exercises.
Patient education and self-management plans.
Conclusion
Allergic rhinitis and bronchial asthma are closely related conditions sharing similar
immunological pathways. Both are driven by IgE-mediated hypersensitivity, mast cell
degranulation, and chronic airway inflammation. Effective management requires a multifaceted
approach including allergen avoidance, pharmacological treatment, and immunotherapy. Recent
advances in biologics offer promising options for patients with severe, uncontrolled asthma and
persistent allergic rhinitis. An integrated treatment strategy not only relieves symptoms but also
improves long-term prognosis and quality of life.
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