Effects of prednisone on the cellular responses and release of cytokines and mediators after segmental allergen challenge of asthmatic subjects
Summary
This summary is machine-generated.Prednisone effectively reduces airway inflammation in asthma by suppressing inflammatory cell recruitment and cytokine production. This systemic glucocorticoid therapy offers a significant benefit for managing allergic airway inflammation.
Area Of Science
- Immunology
- Pulmonology
- Pharmacology
Background
- Systemic glucocorticoids are a primary treatment for allergic inflammation and asthma.
- In vivo data on their specific effects remain limited.
Purpose Of The Study
- To investigate the in vivo effects of prednisone on inflammatory mediators, cytokines, and cellular responses.
- To analyze prednisone's impact in a segmental allergen challenge (SAC) model of allergic asthma.
Main Methods
- A double-blind, placebo-controlled, crossover study involving 10 allergic asthmatic subjects.
- 3-day pretreatment with oral prednisone (30 mg twice daily) followed by SAC.
- Assessment of physiologic and inflammatory responses post-challenge.
Main Results
- Prednisone improved baseline FEV(1) and modestly inhibited the SAC-induced fall in FEV(1).
- It did not inhibit early mediator release (histamine, PGD(2), etc.) but suppressed later inflammatory cell influx (eosinophils, basophils, T lymphocytes).
- Prednisone reduced soluble E-selectin, kinins, albumin, and inhibited T(H)2 cytokine (IL-4, IL-5) and IL-2 mRNA/protein expression.
Conclusions
- Prednisone effectively suppresses multiple aspects of allergic airway inflammation.
- Key suppressed components include inflammatory cell recruitment, adhesion molecule expression, airway permeability, and cytokine production.
- These findings highlight prednisone's role in managing allergic airway inflammation and potentially airway remodeling.
View abstract on PubMed