Monitoring Airway Hyperresponsiveness: Indirect Stimuli— Exercise, Hypertonic Saline, Mannitol, and Adenosine Monophosphate

2005 ◽  
pp. 303-352
Keyword(s):  
Hypertonic Saline ◽  
Airway Hyperresponsiveness ◽  
Adenosine Monophosphate

scholarly journals Calcium-sensing receptor antagonists abrogate airway hyperresponsiveness and inflammation in allergic asthma

2015 ◽  
Vol 7 (284) ◽  
pp. 284ra60-284ra60 ◽  
Author(s):  
Polina L. Yarova ◽  
Alecia L. Stewart ◽  
Venkatachalem Sathish ◽  
Rodney D. Britt ◽  
Michael A. Thompson ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Airway Hyperresponsiveness ◽  
Eosinophil Cationic Protein ◽  
Adenosine Monophosphate ◽  
Asthma Severity ◽  
Mitogen Activated Protein Kinase ◽  
Calcium Sensing Receptor ◽  
Cationic Protein ◽  
Calcium Sensing

Airway hyperresponsiveness and inflammation are fundamental hallmarks of allergic asthma that are accompanied by increases in certain polycations, such as eosinophil cationic protein. Levels of these cations in body fluids correlate with asthma severity. We show that polycations and elevated extracellular calcium activate the human recombinant and native calcium-sensing receptor (CaSR), leading to intracellular calcium mobilization, cyclic adenosine monophosphate breakdown, and p38 mitogen-activated protein kinase phosphorylation in airway smooth muscle (ASM) cells. These effects can be prevented by CaSR antagonists, termed calcilytics. Moreover, asthmatic patients and allergen-sensitized mice expressed more CaSR in ASMs than did their healthy counterparts. Indeed, polycations induced hyperreactivity in mouse bronchi, and this effect was prevented by calcilytics and absent in mice with CaSR ablation from ASM. Calcilytics also reduced airway hyperresponsiveness and inflammation in allergen-sensitized mice in vivo. These data show that a functional CaSR is up-regulated in asthmatic ASM and targeted by locally produced polycations to induce hyperresponsiveness and inflammation. Thus, calcilytics may represent effective asthma therapeutics.

Relationship between airway hyperresponsiveness to mannitol and adenosine monophosphate

Allergy ◽  
2003 ◽  
Vol 58 (8) ◽  
pp. 762-766 ◽  
Author(s):  
G. P. Currie ◽  
K. Haggart ◽  
J. D. Brannan ◽  
D. K. C. Lee ◽  
S. D. Anderson ◽  
...  
Keyword(s):  
Airway Hyperresponsiveness ◽  
Adenosine Monophosphate

scholarly journals Airway Hyperresponsiveness to Hypertonic Saline as a Predictive Index of Exercise-Induced Bronchoconstriction

2005 ◽  
Vol 20 (4) ◽  
pp. 284 ◽  
Author(s):  
Inseon S. Choi ◽  
Se-Woong Chung ◽  
Youngil I. Koh ◽  
Myoung-Ki Sim ◽  
Seo-Na Hong ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Airway Hyperresponsiveness ◽  
Predictive Index ◽  
Exercise Induced

scholarly journals Lung hyperinflation, perception of bronchoconstriction and airway hyperresponsiveness

2007 ◽  
Vol 30 (1) ◽  
pp. 2 ◽  
Author(s):  
Louis-Philippe Boulet ◽  
Helene Turcotte
Keyword(s):  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Adenosine Monophosphate ◽  
Mild Asthma ◽  
Chest Tightness ◽  
Lung Hyperinflation ◽  
Cell Counts ◽  
Symptom Scores ◽  
Maximum Decrease ◽  
The Mean

Purpose: To compare the influence of underlying airway inflammation and lung hyperinflation on dyspnea during induced bronchoconstriction in subjects with mild asthma (or asymptomatic airway hyperresponsiveness (AAHR). Methods: Fourteen mild asthmatic and 14 AAHR subjects had methacholine and 5'-adenosine monophosphate (AMP) challenges, and induced sputum analysis. Changes in inspiratory capacity (IC) and respiratory symptom scores were measured after challenges. Perception of respiratory symptoms was recorded on a modified Borg scale. Results: The mean baseline FEV1, IC, mean provocative concentration of methacholine inducing a 20% decrease in FEV1 (PC20), the mean PC20 AMP and median inflammatory cell counts were similar in both groups. After methacholine, mean (±SD) reductions in FEV1 were 24.7±10.3% in mild asthma and 35.6±19.1% in AAHR (P>0.05); reductions in IC were, respectively, 10±12% and 24±20% (P>0.05); mean breathlessness scores at PC20 were 1.1 in mild asthma and 0 in AAHR P=0.003), and mean chest tightness scores were 1.2 in mild asthma and 0.8 in AAHR (P>0.05). Maximum chest tightness scores following MC correlated with the maximum decrease in IC in mild asthma (rs=0.75,P=0.009) and with the maximum decrease in FEV1 in AAHR (rs=0.60,P=0.04). After AMP, symptom scores were not significantly correlated with decreases in FEV1 or IC. The number of inflammatory cells was not correlated with decreases in IC after methacholine, AMP or with their PC20s, although inflammation was minimal in both groups. Conclusion: Lower breathlessness scores in AAHR compared to mild asthma were not explained by differences in lung hyperinflation nor in airway inflammation.

scholarly journals Asthmatic Airway Inflammation is More Closely Related to Airway Hyperresponsiveness to Hypertonic Saline than to Methacholine

2003 ◽  
Vol 18 (2) ◽  
pp. 83-88 ◽  
Author(s):  
Inseon S. Choi ◽  
Seo-Na Hong ◽  
Yeon-Kyung Lee ◽  
Youngil I. Koh ◽  
An-Soo Jang ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Hypertonic Saline ◽  
Airway Hyperresponsiveness ◽  
Asthmatic Airway

Elucidating cyclic AMP signaling in subcellular domains with optogenetic tools and fluorescent biosensors

2019 ◽  
Vol 47 (6) ◽  
pp. 1733-1747 ◽  
Author(s):  
Christina Klausen ◽  
Fabian Kaiser ◽  
Birthe Stüven ◽  
Jan N. Hansen ◽  
Dagmar Wachten
Keyword(s):  
Cyclic Amp ◽  
Adenosine Monophosphate ◽  
Adenylyl Cyclases ◽  
Temporal Precision ◽  
Fluorescent Biosensors ◽  
Subcellular Domains ◽  
Spatio Temporal ◽  
Hydrolysis Of ◽  
Shed Light ◽  
Cyclic Amp Signaling

The second messenger 3′,5′-cyclic nucleoside adenosine monophosphate (cAMP) plays a key role in signal transduction across prokaryotes and eukaryotes. Cyclic AMP signaling is compartmentalized into microdomains to fulfil specific functions. To define the function of cAMP within these microdomains, signaling needs to be analyzed with spatio-temporal precision. To this end, optogenetic approaches and genetically encoded fluorescent biosensors are particularly well suited. Synthesis and hydrolysis of cAMP can be directly manipulated by photoactivated adenylyl cyclases (PACs) and light-regulated phosphodiesterases (PDEs), respectively. In addition, many biosensors have been designed to spatially and temporarily resolve cAMP dynamics in the cell. This review provides an overview about optogenetic tools and biosensors to shed light on the subcellular organization of cAMP signaling.

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