Allergic Rhinitis Pathogenesis: A Dysfunctional Cytokine Network

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Allergic rhinitis is an important common disease in otorhinolaryngology. Studies have calculated that the prevalence of this disease in adults in Western countries is 10% to 20%, and the prevalence in Americans is 15% to 18%. In some areas, it can be as high as 30% or more. The pathogenesis of allergic rhinitis should be comprehensively analyzed and investigated from the perspectives of pathophysiology, immunopathology, and molecular immunology, so as to provide a corresponding objective basis for clinical diagnosis and treatment of patients.

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1 Types of allergic rhinitis

Allergic rhinitis is often divided into seasonal allergic rhinitis (also known as grass fever or hay fever) and perennial allergic rhinitis. Among the total allergic rhinitis patients, about 20% are seasonal allergic rhinitis, 40% are perennial allergic rhinitis, and the remaining 40% are mixed allergic rhinitis of the former two. In 2001, 37 experts were organized to summarize the current research status of allergic rhinitis and wrote the article "Allergic Rhinitis and Its Influence on Asthma", which was recommended as allergic rhinitis in the name of WHO Reference standard for clinical assessment and treatment. In this article, according to the characteristics of the disease and its symptoms, allergic rhinitis is divided into two types: intermittent and persistent. Four subtypes of allergic rhinitis can be formed after cross-combination. In the text, the correlation between allergic rhinitis and asthma is also highlighted.

For patients with allergic rhinitis, we should pay attention to and evaluate the occurrence of asthma. Among people with allergic rhinitis, the risk of developing asthma in the future is 4 times that of those without allergic rhinitis; on the contrary, 70% to 80% of asthmatic patients with allergic rhinitis, therefore, we should also pay attention to allergic rhinitis for asthma patients. At the same time prevent and treat inflammation of the upper and lower respiratory tract, improving the treatment plan of asthma or allergic rhinitis, especially the active treatment of allergic rhinitis, can effectively prevent the occurrence or recurrence of asthma.

When the inflammation of allergic rhinitis is limited to the upper respiratory tract, effective treatment measures should be taken to prevent the inflammation from spreading to the lower respiratory tract and causing asthma. Treatment measures include specific immunotherapy, nasal inhalation of glucocorticoids, oral allergy drugs, and immunomodulators. Studies have shown that allergic rhinitis is an important risk factor for asthma, and asthma attacks in children (especially preschool children) are often related to colds. Improving the immune function of children is an effective measure to relieve allergic diseases. The two-way immunomodulator Fuketo (spleen amino-peptide oral freeze-dried powder) can improve the immune function of children and effectively treat allergic rhinitis and asthma. It has a wide range of clinical applications, is convenient to take, has a light taste, and is more suitable for children. Phuket (spleen amino-peptide oral freeze-dried powder) 2 mg/d, used continuously for 60 days, combined with glucocorticoid inhalation, can regulate immune balance, effectively relieve allergic rhinitis, and asthma symptoms, and significantly enhance its cellular immunity and humoral Immune function, effectively improve lung function.

2 Pathogenesis of allergic rhinitis

In recent years, the research on the mechanism of allergic diseases represented by allergic rhinitis has attracted the attention of some well-known scholars at home and abroad. At present, with the basic links of immune cells and inflammatory mediators involved in the immune response being elucidated one by one, the pathogenesis of patients with allergic rhinitis will become clearer.

1 Immune response modulation by cytokine networks

At the beginning of the 20th century, RICH and LEWIS discovered that cell products can affect the biological activities of other cells; after a gap of 40 years, this cell product was named lymphokine; and the related concept of cytokines was formally proposed. Cytokines refer to active substances that can play a variety of regulatory effects on the immune system and the inflammatory response process. They are derived from the secretion of immune cells, vascular endothelial cells, and epithelial cells in the body.

At present, cytokines can be roughly divided into lymphokines, pro-inflammatory cytokines, chemotactic cytokines, anti-inflammatory cytokines, growth factors, and the like according to their biological functions. In allergic inflammatory response, CD4+ T cells play a central role, which can regulate acute or chronic allergic inflammatory responses by releasing a series of cytokines, which can make patients experience acute immediate response and chronically delayed response, respectively. Symptoms of Hairstyle Reactions.

2 Basic immune responses

In the 1970s, the basic immune response process of allergic rhinitis has been clarified, that is, due to the combination of allergens by anti-presenting cells and IgE antibodies on the surface of mast cells, resulting in degranulation of mast cells and the release of inflammatory response mediators, which makes the patient Symptoms of an allergic reaction. Further research found that the allergic reaction process is composed of two stages: immediate response (APR) and delayed response (LPR).

(1) Immediate response: Individuals sensitized by allergens can have an immediate response within a few minutes under the continuous stimulation of the antigen, and mast cells play a central role in this stage. IgE-encapsulated mast cells increase, resulting in the degranulation of allergens deposited in the respiratory mucosa, and the release of inflammatory mediators such as histamine, protease, chymase, kininogenase, and heparin in the granules; at the same time, Mast cells can also secrete prostaglandin D₂, leukotriene C4, leukotriene D4, leukotriene E4, and other inflammatory mediators. Allergic rhinitis produces a large number of inflammatory mediators, which can cause nasal itching, eye itching, watery itching, continuous sneezing, and various degrees of nasal congestion.

(2) Delayed-type reaction: After 6 to 9 hours of contact with the allergen, the delayed-type reaction can reach a peak, and then gradually reduce or disappear. During this period, the inflammatory mediators produced by mast cells mainly act on vascular endothelial cells, express vascular cell adhesion molecule (VCAM) and selectin E, and lead to the adhesion of leukocytes and vascular endothelial cells in the blood circulation. The synergistic participation of cytokines promotes the infiltration of eosinophils, neutrophils, basophils, T cells, and macrophages in the nasal mucosa. Once the inflammatory cells infiltrated in the nasal mucosa are activated, they will release a large number of inflammatory mediators, which may trigger an immediate response again, resulting in the recurrence of acute allergic symptoms. Delayed-type responses can be stimulated by mast cells or T cells. The former depends on the effect of IgE, while the latter does not depend on the effect of IgE, but is mainly mediated by histocompatibility complex (MHC). Based on the clinical manifestations of patients with allergic rhinitis alone, it is usually not easy to distinguish between immediate and delayed reactions, and the only clinical manifestations that can help to distinguish are limited to longer-lasting nasal congestion symptoms that can occur during the delayed reaction stage.