Airway Smooth Muscle Synthesis of Inflammatory Mediators

2008 ◽  
pp. 141-158
Author(s):  
Alison E. John ◽  
Deborah L. Clarke ◽  
Alan J. Knox ◽  
Karl Deacon
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Inflammatory Mediators

Invited Review: Do inflammatory mediators influence the contribution of airway smooth muscle contraction to airway hyperresponsiveness in asthma?

2003 ◽  
Vol 95 (2) ◽  
pp. 844-853 ◽  
Author(s):  
Darren J. Fernandes ◽  
Richard W. Mitchell ◽  
Oren Lakser ◽  
Maria Dowell ◽  
Alastair G. Stewart ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Inflammatory Mediators ◽  
Airway Hyperresponsiveness ◽  
Molecular Mechanisms ◽  
Normal Subjects ◽  
Smooth Muscle Contraction ◽  
Deep Inspiration ◽  
Contractile Apparatus ◽  
Muscle Shortening

It is now accepted that a host of cytokines, chemokines, growth factors, and other inflammatory mediators contributes to the development of nonspecific airway hyperresponsiveness in asthma. Yet, relatively little is known about how inflammatory mediators might promote airway structural remodeling or about the molecular mechanisms by which they might exaggerate smooth muscle shortening as observed in asthmatic airways. Taking a deep inspiration, which provides relief of bronchodilation in normal subjects, is less effective in asthmatic subjects, and some have speculated that this deficiency stems directly from an abnormality of airway smooth muscle and results in airway hyperresponsiveness to constrictor agonists. Here, we consider some of the mechanisms by which inflammatory mediators might acutely or chronically induce changes in the contractile apparatus that in turn might contribute to hyperresponsive airways in asthma.

Pro-inflammatory mediators increase levels of the noncoding RNA GAS5 in airway smooth muscle and epithelial cells

2015 ◽  
Vol 93 (3) ◽  
pp. 203-206 ◽  
Author(s):  
Christine R. Keenan ◽  
Michael J. Schuliga ◽  
Alastair G. Stewart
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Airway Smooth Muscle ◽  
Inflammatory Mediators ◽  
Noncoding Rna ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Structural Cell ◽  
Glucocorticoid Sensitivity

The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway epithelial cells (AEC) play an important role in the pathogenesis and persistence of asthma and other chronic airways diseases. These airway structural cell types are also important cellular targets of the anti-inflammatory actions of glucocorticoids. In this study, we sought to examine the relevance of GAS5 to glucocorticoid sensitivity and resistance in ASM and AEC. We provide the first evidence that pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in AEC.

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