Mechanisms of intranasal steroids in the management of upper respiratory allergic diseases☆,☆☆,★
Section snippets
Eosinophils
The most prominent effector cell in allergic rhinitis and in the late-phase reaction of the nose to allergen challenge is the eosinophil.5 The number of eosinophils, particularly activated eosinophils (EG2+), increases substantially in the epithelium and lamina propria during the allergic response.6 Intranasal steroids reduce eosinophil numbers by inhibiting eosinophil recruitment and migration into the nasal airways and promoting eosinophil apoptosis.7, 8
Clinical studies have confirmed the
DIRECTOR MECHANISMS
The director mechanisms are the forces behind the effector mechanisms. Important components of the director mechanisms include epithelial cells, antigen-presenting cells, and T lymphocytes. In addition, 2 major effector cells, eosinophils and mast cells, contribute as director cells as well through their release of cytokines (Table I).
CONCLUSION
Intranasal steroids reduce the influx of inflammatory cells into the nasal mucosa in response to allergic stimuli. This reduces the release of inflammatory mediators and the development of nasal hyperresponsiveness. The inhibition of allergic inflammation results from the action of corticosteroids in blocking the synthesis and release of cytokines and chemokines from T lymphocytes, epithelial cells, eosinophils, and mast cells. Although attenuation of the allergic inflammatory reaction can be
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Cited by (18)
Foxp3+ T regulatory cells (Tregs) are increased in nasal polyps (NP) after treatment with intranasal steroid
2008, Clinical ImmunologyCitation Excerpt :The exact mechanism is not fully certain. It may extensively affect the inflammatory cells including T cells, B cells, mast cell, eosinophils, and antigen-presenting cells etc.[17], as well as a lot of mediators such as channel protein, growth factor etc. [18,19]. Recently, steroid also has been shown to participate in the expansion of naturally occurred Tregs [20], which may account for its anti-inflammatory effects as a new mechanism.
Pathophysiology and progression of nasal septal perforation
2007, Annals of Allergy, Asthma and ImmunologyNasal carriage of Staphylococcus aureus in children with allergic rhinitis and the effect of intranasal fluticasone propionate treatment on carriage status
2007, International Journal of Pediatric OtorhinolaryngologyCitation Excerpt :Although glucocorticoid use in nasal polyposis has been proposed to increase nasal carriage of MRSA, the actual relation of nasal corticosteroid use and NCSA was largely unknown [11]. Intranasal corticosteroids have broad anti-inflammatory effects and some of these might favor against the NCSA [16,17]. Corticosteroids show an inhibitory effect on fibronectin production, which is one of the proposed binding sites of S. aureus[17].
Pharmacology, particle deposition and drug administration techniques of intranasal corticosteroids for treating allergic rhinitis
2022, Clinical and Experimental AllergyExploring the role of antibiotics and steroids in managing respiratory diseases
2022, Journal of Biochemical and Molecular Toxicology
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Supported by an unrestricted educational grant from Schering/Key Pharmaceuticals, Schering Corporation.
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Reprint requests: Harold S. Nelson, MD, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO 80206.
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