Pathophysiology of Allergic Rhinitis
Allergic rhinitis is more than just a runny nose; it is a complex immune-mediated inflammatory condition that features various biological reactions in the upper respiratory tract.
When someone with a genetic or environmental predisposition inhales airborne allergens like pollen, dust mites, mold spores, or pet dander, the immune system perceives these harmless particles as harmful invaders. This initiates a chain of immunological responses that appear as the symptoms are frequently linked with hay fever.
Sensitization: The First Step
The process of allergic reactions begins with allergen sensitivity. Initially, antigen-presenting cells (APCs), commonly the dendritic cells in the nasal mucosa, capture and process the allergen particles. These cells subsequently deliver allergenic peptides to T-helper type 2 (Th2) lymphocytes that produce cytokines, including IL-4, IL-5, and IL-13.
These cytokines activate B-cells to produce allergen-specific immunoglobulin E (IgE) antibodies. The IgE molecules then adhere to mast cells and basophils, “priming” them for future exposures. Clinically, this period is silent; the person feels no symptoms, but the immune system has been prepared to overreact the next time.
Early-Phase Allergic Reaction
The early-phase reaction happens within minutes of allergen exposure.
When exposed to the same allergen again, mast cell-bound IgE antibodies detect it and cause mast cell degranulation. This causes the release of potent chemical mediators such as histamine, leukotrienes, prostaglandins, and cytokines into the nasal tissue.
These mediators cause:
- acute nasal congestion and swelling by vasodilation and increased vascular permeability
- Itching and sneezing by stimulation of sensory nerves
- Excess mucus and rhinorrhea (runny nose) by glandular secretions.
Late-Phase Inflammatory Response
After a few hours, the late-phase reaction starts.
Inflammatory cells, including eosinophils, basophils, Th2 cells, and group 2 innate lymphoid cells (ILC2s), infiltrate the nasal mucosa. These cells produce more cytokines and harmful proteins, causing inflammation to persist even in the absence of continued allergen contact.
This chronic inflammation causes persistent nasal blockage, sinus pressure, and mucosal edema. Long-term, it can cause tissue remodeling, including fibrosis, goblet cell hyperplasia, and collagen deposition, resulting in a more severe and persistent form of allergic rhinitis.
Neuro-Immune Interactions
A recent study has shown that sensory nerve activity plays a role in the perpetuation of nose symptoms. Nerve endings in the nasal mucosa become hypersensitive, releasing neuropeptides that exacerbate inflammation, resulting in a vicious cycle of sneezing, itching, and congestion. This explains why people with allergic rhinitis are generally more sensitive to irritants like smoke, fragrance, and temperature fluctuations.
Systemic and Lower-Airway Links
In allergic rhinitis, the inflammation spreads beyond the nose. Mediators secreted in the nasal passages can enter the bloodstream and affect the lower airways, which explains the common coexistence of asthma and rhinitis, also known as the “one airway, one disease” notion. Effective allergic rhinitis management can thus help prevent asthma exacerbations and enhance overall respiratory health.
Frequently Asked Questions (FAQs)
1. What is the basic pathophysiology of allergic rhinitis?
Allergic rhinitis is an IgE-mediated inflammatory reaction in the nasal mucosa triggered by inhaled allergens such as pollen, dust mites, pet dander, or mold.
2. What is sensitization in allergic rhinitis?
Sensitization is the initial phase in which allergen exposure leads to Th2 activation, cytokine release, and production of allergen-specific IgE that binds to mast cells and basophils.
3. What happens during the early-phase allergic reaction?
Within minutes of re-exposure, mast cells degranulate and release mediators like histamine, causing sneezing, itching, nasal congestion, and rhinorrhea.
4. What is the late-phase response in allergic rhinitis?
Several hours later, cells such as eosinophils and Th2 lymphocytes infiltrate the mucosa, maintaining inflammation and contributing to persistent nasal blockage and tissue remodeling.
5. How is allergic rhinitis linked to asthma?
Shared inflammatory pathways mean that mediators from the upper airway can affect the lower airway, supporting the “one airway, one disease” concept and explaining the frequent coexistence of asthma and rhinitis.