Nasal hyperreactivity and inflammation in allergic rhinitis

Area of Science:

• Immunology
• Otorhinolaryngology

Background:

• Allergic disease history traces back to 1819 with Bostock's 'summer catarrh', later identified as hay fever caused by pollen.
• Allergy is defined as an adverse physiological event mediated by immunologic reactions, specifically focusing on IgE-dependent reactions in this review.
• Allergic rhinitis, a key manifestation of IgE-dependent reactions, involves complex histopathological features of nasal inflammation.

Purpose of the Study:

• To review the inflammatory cells and mediators implicated in the pathogenesis of perennial allergic rhinitis.
• To provide a comprehensive overview of the cellular and molecular mechanisms underlying allergic nasal inflammation.

Main Methods:

• Review of existing literature on allergic rhinitis and inflammation.
• Identification and description of primary and secondary effector cells involved in the allergic cascade.
• Analysis of inflammatory mediators generated by various cell types in response to stimuli.

Main Results:

• Histopathological features include increased blood flow, vascular permeability, plasma exudation, and edema.
• Both resident nasal cells (mast cells, antigen-presenting cells, epithelial cells) and recruited cells (basophils, eosinophils, lymphocytes, platelets, neutrophils) contribute to inflammation.
• Specific inflammatory mediators are generated by these cells, driving the allergic process in the nose.

Conclusions:

• Allergic rhinitis pathogenesis involves a complex interplay of diverse inflammatory cells and their mediators.
• Understanding these cellular and molecular players is crucial for developing targeted therapies for perennial allergic rhinitis.