This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages before signing in

Go to /pro/cpd-dashboard page

This page is worth 0.05 CPD credits. CPD dashboard

Go to /account/subscription-details page

This page is worth 0.05 CPD credits. Upgrade to Pro

Mechanisms of action

Authoring team

Molecular mechanisms - inhaled glucocorticoids are highly lipophilic. They rapidly enter airway cells and bind to cytosolic receptors. The glucocorticoid-receptor complex then moves into the nucleus and binds to the DNA where they alter gene transcription or modulate gene expression which results in altered protein synthesis (1). The complex may also inhibit the transcription of the genes for cytokines implicated in asthmatic inflammation.

Cellular effects - inhaled steroids may have inhibitory effects on many cells involved in airway inflammation including macrophages, T-lymphocytes, eosinophils, and airway epithelial cells. They may also inhibit plasma exudation and mucus secretion in inflamed airways.

Anti-inflammatory effects - there is a marked anti-inflammatory effect of inhaled glucocorticoids on the bronchial mucosa in patients with asthma.

Effects on airway hyperresponsiveness - inhaled steroids consistently lessen airway hyperresponsiveness in children and adults with asthma.

Reference:


Create an account to add page annotations

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.