Filtered By:
Drug: Flonase

This page shows you your search results in order of date.

Order by Relevance | Date

Total 7 results found since Jan 2013.

Th1 cytokines TNF- α and IFN-γ promote corticosteroid resistance in developing human airway smooth muscle.
Th1 cytokines TNF-α and IFN-γ promote corticosteroid resistance in developing human airway smooth muscle. Am J Physiol Lung Cell Mol Physiol. 2019 Jan 01;316(1):L71-L81 Authors: Britt RD, Thompson MA, Sasse S, Pabelick CM, Gerber AN, Prakash YS Abstract Corticosteroids (CSs) are commonly used to manage wheezing and asthma in pediatric populations. Although corticosteroids are effective in alleviating airway diseases, some children with more moderate-severe asthma phenotypes show CS resistance and exhibit significant airflow obstruction, persistent inflammation, and more frequent exacerbations. Previ...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - December 19, 2018 Category: Cytology Authors: Britt RD, Thompson MA, Sasse S, Pabelick CM, Gerber AN, Prakash YS Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Th1 Cytokines, TNF α and IFNγ, Promote Corticosteroid Resistance in Developing Human Airway Smooth Muscle.
Th1 Cytokines, TNFα and IFNγ, Promote Corticosteroid Resistance in Developing Human Airway Smooth Muscle. Am J Physiol Lung Cell Mol Physiol. 2018 Oct 18;: Authors: Britt RD, Thompson MA, Sasse SK, Pabelick CM, Gerber AN, Prakash YS Abstract Corticosteroids are commonly used to manage wheezing and asthma in pediatric populations. Although corticosteroids are effective in alleviating airway diseases, some children with more moderate-severe asthma phenotypes show corticosteroid (CS) resistance and exhibit significant airflow obstruction, persistent inflammation, and more frequent exacerbations. Previo...
Source: Am J Physiol Lung Ce... - October 18, 2018 Category: Respiratory Medicine Authors: Britt RD, Thompson MA, Sasse SK, Pabelick CM, Gerber AN, Prakash YS Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Protein phosphatase 5 mediates corticosteroid insensitivity in airway smooth muscle in patients with severe asthma
ConclusionsPP5‐dependent impairment of GRα function represents a novel mechanism driving GC insensitivity in ASM in severe asthma.This article is protected by copyright. All rights reserved.
Source: Allergy - August 9, 2016 Category: Allergy & Immunology Authors: Latifa Chachi, Mahnaz Abbassian, Adelina Gavrila, Abdulrahman Alzahrani, Omar Tliba, Peter Bradding, Andrew J. Wardlaw, Christopher Brightling, Yassine Amrani Tags: Original Article: Airway Diseases Source Type: research

Role of protein phosphatase 5 (PP5) in mediating corticosteroid insensitivity in airway smooth muscle (ASM) cells in severe asthma
Although the mechanisms mediating corticosteroid resistance in severe asthma are still unknown, recent evidence suggests ASM cells isolated from patients with severe asthma have a decreased insensitivity to dexamethasone (Dex) with respect to the inhibition of chemokine production. Here we investigated whether this corticosteroid insensitivity seen in ASM from severe asthmatics was due to an abnormal GR signalling pathway. We here observed that production of CCL5 and CCL11 by TNF in ASM cells from severe asthmatics (compared to healthy subjects and nonsevere asthma) was not affected by Dex or fluticasone (FP) pretreatment....
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Chachi, L., Abbasian, M., Gavrila, A., Tliba, O., Brightling, C., Amrani, Y. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

Compound A modulates steroid insensitive chemokines in airway smooth muscle cells via IRF-1 dependent and independent pathways
In conclusion, CpdA suppresses production of GC-resistant chemokines via IRF-1 dependent and independent mechanisms.Targeting CpdA sensitive pathways in ASM cells represents an alternative therapeutic approach for GC insensitivity treatment in asthma.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Gavrila, A., Chachi, L., Tliba, O., Brightling, C., Amrani, Y. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research

The Plant Derivative Compound A Inhibits the Production of Corticosteroid-resistant Chemokines by Airway Smooth Muscle Cells.
Abstract Preclinical models of human conditions including asthma showed the therapeutic potential of compound A (CpdA), a dissociated glucocorticoid (GC) receptor (GRα) ligand. Whether CpdA inhibits GC resistance, a central feature of severe asthma, has not been addressed. We investigated whether CpdA modulates cytokine-induced GC resistance in human airway smooth muscle (ASM) cells. Healthy and asthmatic ASM cells were treated with TNFα/IFNγ for 24 hr in the presence or absence of CpdA. ELISA and qPCR assays were used to assess the effect of CpdA on chemokine expression. Activation of GRα by CpdA was assessed...
Source: Am J Respir Cell Mol... - April 21, 2015 Category: Respiratory Medicine Authors: Gavrila A, Chachi L, Tliba O, Brightling C, Amrani Y Tags: Am J Respir Cell Mol Biol Source Type: research

Basal p38 MAPK Regulates Unliganded Glucocorticoid Receptor Function in Airway Smooth Muscle Cells.
Abstract Like many other steroid receptors, the glucocorticoid (GC) receptor (GR) is a phospho-protein. Although there are multiple phosphorylation sites critical for GR transcriptional activity, i.e. serines 203 (S203), 211 (S211), and 226 (S226), their respective role in driving GR functions is highly cell specific. We have recently identified PP5 as an essential Ser/Thr phosphatase responsible for impairing GR function via S211 dephosphorylation in airway smooth muscle (ASM) cells (Am J Respir Cell Mol Biol. 2012 Oct;47(4):464-73). Because p38 MAPK directly phosphorylates GR in different cell types in a stimulu...
Source: Am J Respir Cell Mol... - September 11, 2013 Category: Respiratory Medicine Authors: Bouazza B, Debba-Pavard M, Amrani Y, Isaacs L, O'Connell D, Ahamed S, Formella D, Tliba O Tags: Am J Respir Cell Mol Biol Source Type: research